TIM SPECIFI CONTENT TEACHIN EVALUA

E C G TION
OBJECTI LEARNIN
VE G
ACTIVITIE
S
INTRODU
CTION:
The feet
are the
foundation
of our
bodies,
and they
assist us in
some of
the most
basic
functions
of living.
Each foot
contains
26 bones,
which are
controlled
by
multiple
ligaments,
muscles,
and
tendons.[1]
Through
activities
of living,
the feet
can
change
structurall
y over
time,
causing a
reshaping
of the feet.
This can
 give rise to
a number
of medical
conditions
and
deformitie
s. In
addition,
the feet
are
susceptibl
e to
infections
including
bacterial,
fungal,
and viral
infections.
Systemic
illnesses
can also
affect and
change
the feet,
which can
limit daily
activity
and
quality of
life.

20m To COMMON DISORDERS OF FOOT: Student Discusse

in discuss [A] ARCH DISORDERS: teacher d
about 1)FLAT FEET: describes various
various Flat feet (also called pes planus or various foot
foot fallen arches) is a postural deformity in foot disorder
disorders which the arches of the foot collapse, with disorders s
the entire sole of the foot coming into using
complete or near-complete contact with powerpoin
the ground. Some individuals (an t
estimated 2030% of the general presentati
population) have an arch that simply on
never develops in one foot (unilaterally)
or both feet (bilaterally).
There is a functional relationship between
the structure of the arch of the foot and
the biomechanics of the lower leg. The
arch provides an elastic, springy
connection between the forefoot and the
hind foot. This association safeguards so
that a majority of the forces incurred
during weight bearing of the foot can be
dissipated before the force reaches the
long bones of the leg and thigh.[1]
In pes planus, the head of the talus bone
is displaced medially and distal from the
navicular. As a result, the spring ligament
and the tendon of the tibialis posterior
muscle are stretched, so much so that the
individual with pes planus loses the
function of the medial longitudinal arch
(MLA). If the MLA is absent or
nonfunctional in both the seated and
standing positions, the individual has
rigid flatfoot. If the MLA is present and
functional while the individual is sitting or
standing up on their toes, but this arch
disappears when assuming a foot-flat
stance, the individual has supple
flatfoot. This latter condition can be
correctable with well-fitting arch supports.
[1]

Three studies (see citations below in

military section) of military recruits have
shown no evidence of later increased
injury, or foot problems, due to flat feet,
in a population of people who reach
military service age without prior foot
problems. However, these studies cannot
be used to judge possible future damage
from this condition when diagnosed at
younger ages. They also cannot be
applied to persons whose flat feet are
associated with foot symptoms, or certain
symptoms in other parts of the body
(such as the leg or back) possibly
referable to the foot.
The appearance of flat feet is normal and
common in infants, partly due to "baby
fat" which masks the developing arch and
partly because the arch has not yet fully
developed. The human arch develops in
infancy and early childhood as part of
normal muscle, tendon, ligament and
bone growth. Training of the feet,
especially by foot gymnastics and going
barefoot on varying terrain, can facilitate
the formation of arches during childhood,
with a developed arch occurring for most
by the age of four to six years. Flat arches
in children usually become proper arches
and high arches while the child
progresses through adolescence and into
adulthood.
Because young children are unlikely to
suspect or identify flat feet on their own,
it is a good idea for parents or other adult
caregivers to check on this themselves.
Besides visual inspection, parents should
notice whether a child begins to walk
oddly or clumsily, for example on the
outer edges of the feet, or to limp, during
long walks, and to ask the child whether
he or she feels foot pain or fatigue during
such walks. Children who complain about
calf muscle pains, arch pain, or any other
pains around the foot area may be
developing or have flat feet. Pain or
discomfort may also develop in the knee
joints. A recent randomized controlled
trial found no evidence for the efficacy of
treatment of flat feet in children either for
expensive prescribed orthoses (shoe
inserts) or less expensive over-the-
counter orthoses.[2]
As a symptom itself, flat feet usually
accompany genetic musculoskeletal
conditions such as dyspraxia,[3]
ligamentous laxity or hypermobility.

Pathophysiology
Research has shown that tendon specimens from
people who suffer from adult acquired flat feet
show evidence of increased activity of
proteolytic enzymes. These enzymes can break
down the constituents of the involved tendons
and cause the foot arch to fall. In the future,
these enzymes may become targets for new drug
therapies

Diagnosis
Many medical professionals can diagnose
a flat foot by examining the patient
standing or just looking at them. On going
up onto tip toe the deformity will correct
when this is a flexible flat foot in a child
with lax joints. Such correction is not seen
in adults with a rigid flat foot.
An easy and traditional home diagnosis is
the "wet footprint" test, performed by
wetting the feet in water and then
standing on a smooth, level surface such
as smooth concrete or thin cardboard or
heavy paper. Usually, the more the sole of
the foot that makes contact (leaves a
footprint), the flatter the foot. In more
extreme cases, known as a kinked
flatfoot, the entire inner edge of the
footprint may actually bulge outward,
where in a normal to high arch this part of
the sole of the foot does not make contact
with the ground at all.
Treatment
Most flexible flat feet are asymptomatic,
and do not cause pain. In these cases,
there is usually no cause for concern. Flat
feet were formerly a physical-health
reason for service-rejection in many
militaries. However, three military studies
on asymptomatic adults (see section
below), suggest that persons with
asymptomatic flat feet are at least as
tolerant of foot stress as the population
with various grades of arch.
Asymptomatic flat feet are no longer a
service disqualification in the U.S. military.
[citation needed]

In a study performed to analyze the

activation of the tibialis posterior muscle
in adults with pes planus, it was noted
that the tendon of this muscle may be
dysfunctional and lead to disabling
weightbearing symptoms associated with
acquired flat foot deformity. The results of
the study indicated that while barefoot,
subjects activated additional lower-leg
muscles to complete an exercise that
resisted foot adduction. However, when
the same subjects performed the exercise
while wearing arch supporting orthotics
and shoes, the tibialis posterior was
selectively activated. [7] Such discoveries
suggest that the use of shoes with
properly fitting, arch-supporting orthics
will enhance selective activation of the
tibialis posterior muscle thus, acting as an
adequate treatment for the undesirable
symptoms of pes planus.[8]
Rigid flatfoot, a condition where the sole
of the foot is rigidly flat even when a
person is not standing, often indicates a
significant problem in the bones of the
affected feet, and can cause pain in about
a quarter of those affected.[9][10] Other
flatfoot-related conditions, such as various
forms of tarsal coalition (two or more
bones in the midfoot or hindfoot
abnormally joined) or an accessory
navicular (extra bone on the inner side of
the foot) should be treated promptly,
usually by the very early teen years,
before a child's bone structure firms up
permanently as a young adult. Both tarsal
coalition and an accessory navicular can
be confirmed by X-ray. Rheumatoid
arthritis can destroy tendons in the foot
(or both feet) which can cause this
condition, and untreated can result in
deformity and early onset of osteoarthritis
of the joint. Such a condition can cause
severe pain and considerably reduced
ability to walk, even with orthoses. Ankle
fusion is usually recommended.[citation needed]
Treatment of flat feet may also be
appropriate if there is associated foot or
lower leg pain, or if the condition affects
the knees or the lower back. Treatment
may include using orthoses such as an
arch support, foot gymnastics or other
exercises as recommended by a
podiatrist/orthotist or physical therapist.
In cases of severe flat feet, orthoses
should be used through a gradual process
to lessen discomfort. Over several weeks,
slightly more material is added to the
orthosis to raise the arch. These small
changes allow the foot structure to adjust
gradually, as well as giving the patient
time to acclimatise to the sensation of
wearing orthoses. Once prescribed,
orthoses are generally worn for the rest of
the patient's life. In some cases, surgery
can provide lasting relief, and even create
an arch where none existed before; it
should be considered a last resort, as it is
usually very time consuming and costly.[11]

2)HIGH ARCHES/PES CAVUS:

Pes cavus (in medical terminology, also

high instep, high arch, talipes cavus,
cavoid foot, and supinated foot type)
is a human foot type in which the sole of
the foot is distinctly hollow when bearing
weight. That is, there is a fixed plantar
flexion of the foot. A high arch is the
opposite of a flat foot and is somewhat
less common.

Types
The term pes cavus encompasses a broad
spectrum of foot deformities. Three main
types of pes cavus are regularly described
in the literature: pes cavovarus, pes
calcaneocavus, and pure pes cavus. The
three types of pes cavus can be
distinguished by their aetiology, clinical
signs and radiological appearance. [2][3]
Pes cavovarus, the most common type
of pes cavus, is seen primarily in
neuromuscular disorders such as Charcot-
Marie-Tooth disease and, in cases of
unknown aetiology, is conventionally
termed idiopathic.[4] Pes cavovarus
presents with the calcaneus in varus, the
first metatarsal plantarflexed, and a claw-
toe deformity.[5] Radiological analysis of
pes cavus in Charcot-Marie-Tooth disease
shows the forefoot is typically
plantarflexed in relation to the rearfoot. [6]
In the pes calcaneocavus foot, which is
seen primarily following paralysis of the
triceps surae due to poliomyelitis, the
calcaneus is dorsiflexed and the forefoot
is plantarflexed.[7] Radiological analysis of
pes calcaneocavus reveals a large talo-
calcaneal angle.
In pure pes cavus, the calcaneus is
neither dorsiflexed nor in varus and is
highly arched due to a plantarflexed
position of the forefoot on the rearfoot. [8]
A combination of any or all of these
elements can also be seen in a
combined type of pes cavus that may be
further categorized as flexible or rigid.[9]
Despite various presentations and
descriptions of pes cavus, not all
incarnations are characterised by an
abnormally high medial longitudinal arch,
gait disturbances, and resultant foot
pathology.

Epidemiology
There are few good estimates of
prevalence for pes cavus in the general
community. While pes cavus has been
reported in between 2 and 29% of the
adult population, there are several
limitations of the prevalence data
reported in these studies.[10] Population-
based studies suggest the prevalence of
the cavus foot is approximately 10%.[11]

Cause
Pes cavus may be hereditary or acquired,
and the underlying cause may be
neurological, orthopedic, or
neuromuscular. Pes cavus is sometimes
but not alwaysconnected through
Hereditary Motor and Sensory Neuropathy
Type 1 (Charcot-Marie-Tooth disease) and
Friedreich's Ataxia; many other cases of
pes cavus are natural.
The cause and deforming mechanism
underlying pes cavus is complex and not
well understood. Factors considered
influential in the development of pes
cavus include muscle weakness and
imbalance in neuromuscular disease,
residual effects of congenital clubfoot,
post-traumatic bone malformation,
contracture of the plantar fascia, and
shortening of the Achilles tendon.[12]
Among the cases of neuromuscular pes
cavus, 50% have been attributed to
Charcot-Marie-Tooth disease,[13] which is
the most common type of inherited
neuropathy with an incidence of 1 per
2,500 persons affected.[14] Also known as
Hereditary Motor and Sensory Neuropathy
(HMSN), it is genetically heterogeneous
and usually presents in the first decade of
life with delayed motor milestones, distal
muscle weakness, clumsiness, and
frequent falls. By adulthood, Charcot-
Marie-Tooth disease can cause painful foot
deformities such as pes cavus. Although it
is a relatively common disorder affecting
the foot and ankle, little is known about
the distribution of muscle weakness,
severity of orthopaedic deformities, or
types of foot pain experienced. There are
no cures or effective courses of treatment
to halt the progression of any form of
Charcot-Marie-Tooth disease.[15]
The development of the cavus foot
structure seen in Charcot-Marie-Tooth
disease has been previously linked to an
imbalance of muscle strength around the
foot and ankle. A hypothetical model
proposed by various authors describes a
relationship whereby weak evertor
muscles are overpowered by stronger
invertor muscles, causing an adducted
forefoot and inverted rearfoot. Similarly,
weak dorsiflexors are overpowered by
stronger plantarflexors, causing a
plantarflexed first metatarsal and anterior
pes cavus.[16]
Pes cavus is also evident in people
without neuropathy or other neurological
deficit. In the absence of neurological,
congenital, or traumatic causes of pes
cavus, the remaining cases are classified
as being idiopathic because their
aetiology is unknown.[17]

Pain and disability

As with certain cases of flat feet, high
arches may be painful due to metatarsal
compression; however, high arches
particularly if they are flexible or properly
cared-formay be an asymptomatic
condition.[citation needed]
People with pes cavus sometimes
though not alwayshave difficulty finding
shoes that fit and may require support in
their shoes. Children with high arches who
have difficulty walking may wear
specially-designed insoles, which are
available in various sizes and can be
made to order.
Individuals with pes cavus frequently
report foot pain, which can lead to a
significant limitation in function. The
range of complaints reported in the
literature include metatarsalgia, pain
under the first metatarsal, plantar
fasciitis, painful callosities, ankle arthritis,
and Achilles tendonitis.[18]
There are many other symptoms believed
to be related to the cavus foot. These
include shoe-fitting problems,[19] lateral
ankle instability,[20] lower limb stress
fractures,[21] knee pain,[22] iliotibial band
friction syndrome,[23] back pain [24] and
tripping.[25]
Foot pain in people with pes cavus may
result from abnormal plantar pressure
loading because, structurally, the cavoid
foot is regarded as being rigid and non-
shock absorbent and having reduced
ground contact area. There have
previously been reports of an association
between excessive plantar pressure and
foot pathology in people with pes cavus.
[26]

Treatment
Surgical treatment is only initiated if there
is severe pain, as the available operations
can be difficult. Otherwise, high arches
may be handled with care and proper
treatment.
Suggested conservative management of
patients with painful pes cavus typically
involves strategies to reduce and
redistribute plantar pressure loading with
the use of foot orthoses and specialised
cushioned footwear.[27][28] Other non-
surgical rehabilitation approaches include
stretching and strengthening of tight and
weak muscles, debridement of plantar
callosities, osseous mobilization,
massage, chiropractic manipulation of the
foot and ankle, and strategies to improve
balance.[29] There are also numerous
surgical approaches described in the
literature that are aimed at correcting the
deformity and rebalancing the foot.
Surgical procedures fall into three main
groups:

1. soft-tissue procedures (e.g. plantar

fascia release, Achilles tendon
lengthening, tendon transfer);

2. osteotomy (e.g. metatarsal,

midfoot or calcaneal);

3. bone-stabilising procedures (e.g.

triple arthrodesis

[B]BONE DISORDERS:
1) Sesamoiditis is pain at the sesamoid
bones beneath the head of the 1st
metatarsal, with or without inflammation
or fracture. Diagnosis is usually clinical.
Treatment is usually modification of
footwear and orthotics.
Bones of the foot.

Sesamoiditis is a common cause of

metatarsalgia. The 2 semilunar-shaped
sesamoid bones aid the foot in
locomotion. The medial bone is the tibial
sesamoid, and the lateral bone is the
fibular sesamoid. Direct trauma or
positional change of the sesamoids due to
alterations in foot structure (eg, lateral
displacement of a sesamoid due to lateral
deviation of the great toe) can make the
sesamoids painful. Sesamoiditis is
particularly common among dancers,
joggers, and people who have high-arched
feet or wear high heels. Many people with
bunions have tibial sesamoiditis.

Symptoms and Signs

The pain of sesamoiditis is beneath the
head of the 1st metatarsal; the pain is
usually made worse by ambulation and
may be worse when wearing flexible thin-
soled or high-heeled shoes. Occasionally,
inflammation occurs, causing mild warmth
and swelling or occasionally redness that
may extend medially and appear to
involve the 1st metatarsophalangeal joint.
Sesamoid fracture can also cause pain,
moderate swelling, and possibly
inflammation.

Diagnosis
Clinical evaluation
Arthrocentesis if there is
circumferential joint swelling
Imaging if fracture, osteoarthritis,
or displacement is suspected
With the foot and 1st (big) toe dorsiflexed,
the examiner inspects the metatarsal
head and palpates each sesamoid.
Tenderness is localized to a sesamoid,
usually the tibial sesamoid.
Hyperkeratotic tissue may indicate that a
wart or corn is causing pain. If
inflammation causes circumferential
swelling around the 1st
metatarsophalangeal joint, arthrocentesis
is usually indicated to exclude gout and
infectious arthritis. If fracture,
osteoarthritis, or displacement is
suspected, x-rays are taken. Sesamoids
separated by cartilage or fibrous tissue
(bipartite sesamoids) may appear
fractured on x-rays. If plain x-rays are
equivocal, MRI may be done.

Treatment
New shoes, orthotics, or both
Simply not wearing the shoes that cause
pain may be sufficient. If symptoms of
sesamoiditis persist, shoes with a thick
sole and orthotics are prescribed and help
by reducing sesamoid pressure. If fracture
without displacement is present,
conservative therapy may be sufficient
and may also involve immobilization of
the joint with the use of a flat, rigid,
surgical shoe. NSAIDs and injections of a
corticosteroid/local anesthetic solution
can be helpful. Although surgical removal
of the sesamoid may help in recalcitrant
cases, it is controversial because of the
potential for disturbing biomechanics and
mobility of the foot. If inflammation is
present, treatment includes conservative
measures plus local infiltration of a
corticosteroid/anesthetic solution to help
reduce symptoms

2)META TARSAL FRACTURE:

Metatarsal Fracture Explained

Metatarsal fractures are the most
common traumatic foot injuries. Broken
Metatarsals have been prominent across
all professional sports in the past five
years, with several high profile athletes
suffering Metatarsal fractures.
Professional football (soccer) players
David Beckham, Wayne Rooney, Ashley
Cole and Steve Gerrard have all sustained
this foot injury in recent years. To
understand the Metatarsal fractures
further it is probably best to start by
explaining the anatomy of the foot.
There are five Metatarsal bones in each
foot. They are the relatively long bones
which are located between the 'Tarsal'
bones of the hind-foot and the 'Phalanges'
bones in the toes. Functionally, the ankle
and foot have two principle functions:
propulsion and support. The Metatarsal
bones play a major role in these functions.
For propulsion they act like a rigid lever
and for support they act like a flexible
structure that aids balance, thus holding
up the entire body.

Fractures to the Metatarsal bones can be

caused by direct trauma, excessive
rotational forces or overuse. During
football, direct trauma is usually caused
by a player accidentally kicking the sole
of an opponent's boot, or by an opponent
stepping on a player's foot. As there is
very little soft tissue to protect the top of
the foot, bone injuries are common. The
second, third and fourth Metatarsals are
the most commonly fractured with this
mechanism of injury, although the fifth
Metatarsal is fractured more often in
soccer.
The fifth Metatarsal is divided into four
anatomic segments (the base, the
junction of the base and the shaft, the
shaft, and the neck) and different types of
fracture can occur at each segment.

Fractures of the base of the fifth

Metatarsal are the most common fifth
Metatarsal injuries, and occur as a result
of a twisting injury of the foot or ankle.
The ankle rolls inward and there is a
strong ligament that attaches to the base
of the Metatarsal which pulls off a small
bone fragment. This type of fracture is
invariably treated without surgery, and
immediate walking in a removable plastic
cast is ideal.
The junction between the base of the
Metatarsal and the shaft is the area which
creates most problems when fractured.
The reason for the difficulty is that bone
healing relies upon a good circulation, and
this particular area of the bone has a
notoriously poor blood supply. Fractures of
the shaft of the Metatarsal occur
commonly as a result of twisting of the
foot when landing from a jump, for
example in ballet dancers, and these heal
very rapidly with immobilisation, without
any need for surgery.
Overuse can cause stress
fractures of the Metatarsals.
These fractures are common in
army recruits as well as
sporting individuals and are
commonly known as 'march'
fractures. The patient will
normally report about two
weeks of gradually increasing
pain in the region before an
incident 'converts' the stress
fracture to a full fracture. The
second Metatarsal is the most
commonly affected, but the
fifth Metatarsal can also be
affected. While the stress
fracture of the second
Metatarsal usually heals well,
the healing of a stress fracture
to the fifth MetatarsMetatarsal
Fracture Signs & Symptoms
There is severe foot pain with a
Metatarsal fracture and the patient will
usually find it difficult to walk. Often there
will be pain if the fracture site is touched.
A swollen foot is fairly common and
bruising is usually evident after a day or
two.

lMetatarsal Fracture Treatment

What you can do

Consult a sports injury expert

Apply ice packs/cold therapy to reduce

swelling
 Protect the foot with a removable plastic
cast

Use a buoyancy aid for pool exercises

Use a bone healing system to speed up

broken bone healing

If a Metatarsal fracture is suspected the

patient should be transferred to an
emergency department where a doctor
can confirm the diagnosis by ordering an
x-ray . Immediately following a
Metatarsal fracture ice therapy can be
effective to help with pain relief, although
medication prescribed by a doctor is
usually necessary. Ice Packs for a period
of twenty minutes every couple of hours
may help with the pain. The Aircast Ankle
& Foot Cryo/Cuff is the most effective
method of providing ice therapy. It can
provide continuous ice cold water and
compression for 6 hours and
significantly reduces foot pain and
swelling.
The ultimate treatment of Metatarsal
fractures varies depending on the type
and location of the fracture. If the fracture
is due to direct trauma and the fracture
fragments are well aligned then the
treatment is immobilisation in a
Removable Plastic Cast and non-weight
bearing for 6 - 8 weeks.
The removable plastic cast is better than
a plaster cast, because the boot can be
removed for physiotherapy treatment,
which is aimed at preventing stiffness in
the ankle joint. In addition, cardiovascular
fitness can be maintained by performing
non-weight bearing exercises in a
swimming pool using a Buoyancy Belt.
A removable plastic cast is also usually
adequate for 'march' (stress) fractures of
the second Metatarsal and rotational
fractures of the fifth Metatarsal. However,
stress fractures of the base of the fifth
Metatarsal sometimes show a poor
healing capacity. For this reason, many
orthopaedic consultants now favour
surgical fixation. A small incision is made
on the outside border of the foot and a
small screw is placed down the middle of
the fractured bone. With this method a
return to sporting activity is usually
possible after 6 - 8 weeks.
2)STRESS FRACTURES:
Stress fracture, also known as a
hairline fracture, or fissure fracture, is
a fatigue-induced fracture of the bone
caused by repeated stress over time.
Instead of resulting from a single severe
impact, stress fractures are the result of
accumulated trauma from repeated
submaximal loading, such as running or
jumping. Because of this mechanism,
stress fractures are common overuse
injuries in athletes.[1]
Stress fractures can be described as a
very small sliver or crack in the bone;[2]
and are sometimes referred to as "hairline
fractures". Stress fractures most
frequently occur in weight-bearing bones,
such as the tibia (bone of the lower leg),
metatarsals, and navicular bones (bones
of the foot). Less common are fractures to
the femur, pelvis, and sacrum.[3]

Signs and symptoms

Stress fractures most commonly present
as pain with weight bearing that increases
with exercise or activity. The pain usually
subsides with rest but may be constantly
present with a more serious bone injury.
There is usually an area of localized
tenderness on or near the bone and
generalized swelling to the area.
Percussion or palpation to the bone may
reproduce symptoms.[3]

Causes
Bones are constantly attempting to
remodel and repair themselves, especially
during a sport where extraordinary stress
is applied to the bone. Over time, if
enough stress is placed on the bone that
it exhausts the capacity of the bone to
remodel, a weakened sitea stress
fractureon the bone may appear. The
fracture does not appear suddenly. It
occurs from repeated traumas, none of
which is sufficient to cause a sudden
break, but which, when added together,
overwhelm the osteoblasts that remodel
the bone.
Stress fractures commonly occur in
sedentary people who suddenly
undertake a burst of exercise (whose
bones are not used to the task). They may
also occur in athletes completing high
volume, high impact training, such as
running or jumping sports. Stress
fractures are also commonly reported in
soldiers who march long distances.
Muscle fatigue can also play a role in the
occurrence of stress fractures. In a runner,
each stride normally exerts large forces at
various points in the legs. Each shocka
rapid acceleration and energy transfer
must be absorbed. Both muscles and
bones serve as shock absorbers.
However, the muscles, usually those in
the lower leg, become fatigued after
running a long distance and lose their
ability to absorb shock. As the bones now
experience larger stresses, this increases
the risk of fracture.
Previous stress fractures have been
identified as a risk factor.[4]
Diagnosis
X-rays usually do not show evidence of
new stress fractures, but can be used
several weeks after onset of pain when
the bone begins to remodel. A CT scan,
MRI, or 3-phase bone scan may be more
effective for early diagnosis.[5]
MRI appears to be the most accurate test.
[6]

Prevention
One method of avoiding stress fractures is
to add more stress to the bones. Though
this may seem counter-intuitive (because
stress fractures are caused by too much
stress on the bone), moderate stress
applied to the bone in a controlled
manner can strengthen the bone and
make it less susceptible to a stress
fracture. An easy way to do this is to
follow the runner's rule of increasing
distance by no more than 10 percent per
week. This allows the bones to adapt to
the added stress so they are able to
withstand greater stress in the future.
[citation needed]

Strengthening exercises also help build

muscle strength in the legs.
Strengthening these muscles will prevent
them from becoming fatigued quickly,
allowing them to absorb the strain of
running for longer periods of time. Key
muscles that need strengthening with
lower leg stress fractures are the calves
and the shin muscles. Runners often
suffer from overuse injuries or repetitive
stress injuries.[7] These include stress
fractures, stress reactions, tendinitis,
meniscal tears, ITB Friction syndrome, and
exacerbation of pre-existing arthritis.
Stress fractures, if not diagnosed and
treated, can develop into complete
fractures.
Depending on a variety of factors
(including weight, running surface and
shoe durability), runners should replace
their shoes every 300700 miles to allow
adequate mid-sole cushioning. A change
in running surfaces can also help prevent
stress fractures. However, it is also
argued that cushioning in shoes actually
causes more stress by reducing the
body's natural shock-absorbing action,
increasing the frequency of running
injuries.[8]
During exercise that applies more stress
to the bones, it may help to increase
calcium and vitamin D intake, depending
on the individual. Also, it is important to
monitor diet, because nutrition plays a
vital role in bone development. Some
individuals are at risk of osteoporosis, and
depending on the country in which
medical care is being supplied, there may
be an osteoporosis screening program
available.

Treatment
Rest is the only option for complete
healing of a stress fracture. The amount
of recovery time varies greatly depending
upon the location, severity, the strength
of the body's healing response and an
individual's nutritional intake. Complete
rest and a cast or walking boot are usually
used for a period of four to eight weeks,
although periods of rest of twelve to
sixteen weeks are not uncommon for
more severe stress fractures. After this
period activities may be gradually
resumed, as long as the activities do not
cause pain. While the bone may feel
healed and not hurt during daily activity,
the process of bone remodeling may take
place for many months after the injury
feels healed, and incidences of re-
fracturing the bone are still at significant
risk. Activities such as running or sports
that place additional stress on the bone
should only gradually be resumed. One
general rule is to not increase the volume
of training by more than 10 percent from
one week to the next.
Rehabilitation usually includes muscle
strength training to help dissipate the
forces transmitted to the bones. Bracing
or casting the limb with a hard plastic
walking boot or air cast may also prove
beneficial by taking some stress off the
stress fracture. An air cast has pre-
inflated cells that put light pressure on the
bone, which promotes healing by
increasing blood flow to the area. This
also reduces pain because of the pressure
applied to the bone. If the stress fracture
of the leg or foot is severe enough,
crutches can help by removing stress
from the bone.
With severe stress fractures, surgery may
be needed for proper healing. The
procedure may involve pinning the
fracture site, and rehabilitation can take
up to six (6) months

[C] DIABETIC COMPLICATIONS:

1)DIABETIC FOOT ULCERS:
iabetic foot ulcer is a major
complication of diabetes mellitus, and
probably the major component of the
diabetic foot.
Wound healing is an innate mechanism of
action that works reliably most of the
time. A key feature of wound healing is
stepwise repair of lost extracellular matrix
(ECM) that forms the largest component
of the dermal skin layer.[1] But in some
cases, certain disorders or physiological
insult disturbs the wound healing process.
Diabetes mellitus is one such metabolic
disorder that impedes the normal steps of
the wound healing process. Many studies
show a prolonged inflammatory phase in
diabetic wounds, which causes a delay in
the formation of mature granulation tissue
and a parallel reduction in wound tensile
strength.[2]
Treatment of diabetic foot ulcers should
include: blood sugar control, removing
dead tissue from the wound, dressings,
and removing pressure from the wound
through techniques such as total contact
casting.[3] Surgery in some cases may
improve outcomes.[3] Hyperbaric oxygen
therapy may also help but is expensive.[3]
It occurs in 15% of people with diabetes
and precedes 84% of all diabetes-related
lower-leg amputations.[4]

Risk factors
Risk factors implicated in the
development of diabetic foot ulcers are
diabetic neuropathy, peripheral vascular
disease, cigarette smoking, poor glycemic
control, previous foot ulcerations or
amputations, diabetic nephropathy, and
ischemia of small and large blood vessels.
[5][6]
Diabetic patients often suffer from
diabetic neuropathy due to several
metabolic and neurovascular factors.
Peripheral neuropathy causes loss of pain
or feeling in the toes, feet, legs and arms
due to distal nerve damage and low blood
flow. Blisters and sores appear on numb
areas of the feet and legs such as
metatarso-phalangeal joints, heel region
and as a result pressure or injury goes
unnoticed and eventually become portal
of entry for bacteria and infection.

Pathophysiology
Extracellular matrix
Extra cellular matrix (or "ECM") is the
external structural framework that cells
attach to in multicellular organisms. The
dermis lies below the epidermis, and
these two layers are collectively known as
the skin. Dermal skin is primarily a
combination of fibroblasts growing in this
matrix. The specific species of ECM of
connective tissues often differ chemically,
but collagen generally forms the bulk of
the structure.
Through the interaction of cell with its
extracellular matrix (transmitted through
the anchoring molecules classed as
integrins) there forms a continuous
association between cell interior, cell
membrane and extracellular matrix
components that help drive various
cellular events in a regulated fashion.[7]
Wound healing is a localized event
involving the reaction of cells to the
damage sustained.
The cells break down damaged ECM and
replace it, generally increasing in number
to react to the harm. The process is
activated, though perhaps not exclusively,
by cells responding to fragments of
damaged ECM, and the repairs are made
by reassembling the matrix by cells
growing on and through it. Because of this
extracellular matrix is often considered as
a 'conductor of the wound healing
symphony'.[8] In the Inflammatory phase,
neutrophils and macrophages recruit and
activate fibroblasts which in subsequent
granulation phase migrate into the
wound, laying down new collagen of the
subtypes I and III.
In the initial events of wound healing,
collagen III predominates in the
granulation tissue which later on in
remodeling phase gets replaced by
collagen I giving additional tensile
strength to the healing tissue.[9][10] It is
evident from the known collagen
assembly that the tensile strength is
basically due to fibrillar arrangement of
collagen molecules, which self-assemble
into microfibrils in a longitudinal as well as
lateral manner producing extra strength
and stability to the collagen assembly.[10]
[11]
Metabolically altered collagen is known
to be highly inflexible and prone to break
down, particularly over pressure areas.
Fibronectin is the major glycoprotein
secreted by fibroblasts during initial
synthesis of extracellular matrix proteins.
It serves important functions, being a
chemo-attractant for macrophages,
fibroblasts and endothelial cells.

Basement membrane that

separates epidermis from the
dermal layer and endothelial
basement membrane mainly
contain collagen IV that forms a
sheet and binds to other extra
cellular matrix molecules like
laminin and proteoglycans. In
addition to collagen IV, epidermal
and endothelial basement
membrane also contain laminin,
perlecan and nidogen.[10][11]
Hyaluronic acid, a pure
glycosaminoglycan component is
found in high amounts in damaged
or growing tissues. It stimulates
cytokine production by
macrophages and thus promotes
angiogenesis. In normal skin
chondroitin sulfate proteoglycan is
mainly found in the basement
membrane but in healing wounds
they are up regulated throughout
the granulation tissue especially
during second week of wound
repair, when they provide a
temporary matrix with highly
hydrative capacity.[12] Binding of
growth factors is clearly an
important role of perlecan in wound
healing and angiogenesis. Poor
 wound healing in diabetes mellitus
may be related to perlecan
expression. High levels of glucose
can decrease perlecan expression
in some cells probably through
transcriptional and post-
transcriptional modification.[12][13]
Wound healing phases especially,
granulation, re-epithelization and
remodeling exhibit controlled
turnover of extracellular matrix c

Diagnosis
Identification of diabetic foot in medical
databases, such as commercial claims
and prescription data, is complicated by
the lack of a specific ICD-9 code for
diabetic foot and variation in coding
practices. The following codes indicate
ulcer of the lower limb or foot:

707.1 Ulcer of lower limbs, except

pressure ulcer

707.14 Ulcer of heel and midfoot

707.15 Ulcer of other part of foot

707.19 Ulcer of other part of lower

limb

One or more codes, in combination with a

current or prior diagnosis of diabetes may
be sufficient to conclude diabetic foot:

250.0 Diabetes Mellitus

250.8 Diabetes with other specified

manifestations

Prevention
Steps to prevent diabetic foot ulcers
include frequent review by a foot
specialist, good foot hygiene, diabetic
socks[36][37] and shoes, as well as avoiding
injury.

Foot-care education combined with

increased surveillance can reduce
the incidence of serious foot
lesions.[38]

Footwear
The evidence for special footwear to
prevent foot ulcers is poor as of 2008.[34] A
2000 meta-analysis by the Cochrane
Collaboration concluded that "there is
very limited evidence of the effectiveness
of therapeutic shoes".[39][needs update]
Clinical Evidence reviewed the topic and
concluded "Individuals with significant
foot deformities should be considered for
referral and assessment for customised
shoes that can accommodate the altered
foot anatomy. In the absence of significant
deformities, high quality well fitting non-
prescription footwear seems to be a
reasonable option".[40] National Institute
for Health and Clinical Excellence
concluded that for people at "high risk of
foot ulcers (neuropathy or absent pulses
plus deformity or skin changes or previous
ulcer" that "specialist footwear and
insoles" should be provided.[41]
People with loss of feeling in their feet
should inspect their feet on a daily basis,
to ensure that there are no wounds
starting to develop.[42][43] They should not
walk around barefoot, but use proper
footwear at all times.

Treatment
Foot ulcers in diabetes require
multidisciplinary assessment, usually by
podiatrists, diabetes specialists and
surgeons. Treatment consists of
appropriate bandages, antibiotics (against
pseudomonas aeruginosa,
staphylococcus, streptococcus and
anaerobe strains), debridement, and
arterial revascularisation.
Wound dressings
There are many types of dressings used
to treat diabetic foot ulcers such as
absorptive fillers, hydrogel dressings, and
hydrocolloids.[44] There is no good
evidence that one type of dressing is
better than another for diabetic foot
ulcers.[45] In selecting dressings for chronic
non healing wounds it is recommended
that the cost of the product be taken into
account.[46]
Hydrogel dressings may have shown a
slight advantage over standard dressings,
but the quality of the research is of
concern.[47] Dressings and creams
containing silver have not been properly
studied[48] nor have alginate dressings.[49]
Biologically active bandages that combine
hydrogel and hydrocolloid traits are
available, however more research needs
to be conducted as to the efficacy of this
option over others.[44]
Total contact casting
Total contact casting (TCC) is a specially
designed cast designed to take weight of
the foot (off-loading) in patients with
DFUs. Reducing pressure on the wound by
taking weight of the foot has proven to be
very effective in DFU treatment. DFUs are
a major factor leading to lower leg
amputations among the diabetic
population in the US with 85% of
amputations in diabetics being preceded
by a DFU.[50] Furthermore, the 5 year post-
amputation mortality rate among
diabetics is estimated at around 45% for
those suffering from neuropathic DFUs.[50]
TCC has been used for off-loading DFUs in
the US since the mid-1960s and is
regarded by many practitioners as the
reference standard for off-loading the
bottom surface (sole) of the foot.[51]
TCC helps patients to maintain their
quality of life. By encasing the patients
complete foot including the toes and
lower leg in a specialist cast to
redistribute weight and pressure from the
foot to the lower leg during everyday
movements, patients can remain mobile.
[52]
The manner in which TCC redistributes
pressure protects the wound, letting
damaged tissue regenerate and heal.[53]
TCC also keeps the ankle from rotating
during walking, which helps prevent
shearing and twisting forces that can
further damage the wound.[54]
Effective off loading is a key treatment
modality for DFUs, particularly those
where there is damage to the nerves in
the feet (peripheral neuropathy). Along
with infection management and vascular
assessment, TCC is vital aspect to
effectively managing DFUs.[54] TCC is the
most effective and reliable method for off-
loading DFUs.[55][56][57]
Hyperbaric oxygen
In 2012, a Cochrane review concluded
that for people with diabetic foot ulcers,
hyperbaric oxygen therapy reduced the
risk of amputation and may improve the
healing at 6 weeks.[58][needs update] However,
there was no benefit at one year and the
quality of the reviewed trials was
inadequate to draw strong conclusions. [58]
Negative pressure wound therapy
Main article: Negative pressure wound
therapy
This treatment uses vacuum to remove
excess fluid and cellular waste that
usually prolong the inflammatory phase of
wound healing. Despite a straightforward
mechanism of action, results of negative
pressure wound therapy studies have
been inconsistent. Research needs to be
carried out to optimize the parameters of
pressure intensity, treatment intervals
and exact timing to start negative
pressure therapy in the course of chronic
wound healing.[59]
Other treatments
Ozone therapy - there is only limited and
poor-quality information available
regarding the effectiveness of ozone
therapy for treating foot ulcers in people
with diabetes.[60]
Growth factors - there is some low-quality
evidence that growth factors may
increase the likelihood that diabetic foot
ulcers will heal completely
[C]HEEL PAINS:
1) Achilles Tendinitis
Achilles tendinitis is a common condition
that causes pain along the back of the leg
near the heel.

The Achilles tendon is the largest tendon

in the body. It connects your calf muscles
to your heel bone and is used when you
walk, run, and jump.
Although the Achilles tendon can
withstand great stresses from running and
jumping, it is also prone to tendinitis, a
condition associated with overuse and
degeneration.
Description
Simply defined, tendinitis is inflammation
of a tendon. Inflammation is the body's
natural response to injury or disease, and
often causes swelling, pain, or irritation.
There are two types of Achilles tendinitis,
based upon which part of the tendon is
inflamed.
Noninsertional Achilles tendinitis

Noninsertional Achilles Tendinitis

In noninsertional Achilles tendinitis, fibers
in the middle portion of the tendon have
begun to break down with tiny tears
(degenerate), swell, and thicken.
Tendinitis of the middle portion of the
tendon more commonly affects younger,
active people.

Insertional Achilles Tendinitis

Insertional Achilles tendinitis involves the
lower portion of the heel, where the
tendon attaches (inserts) to the heel
bone.
In both noninsertional and insertional
Achilles tendinitis, damaged tendon fibers
may also calcify (harden). Bone spurs
(extra bone growth) often form with
insertional Achilles tendinitis.
Tendinitis that affects the insertion of the
tendon can occur at any time, even in
patients who are not active.
Insertional Achilles tendinitis
Top of page
Cause
Achilles tendinitis is typically not related
to a specific injury. The problem results
from repetitive stress to the tendon. This
often happens when we push our bodies
to do too much, too soon, but other
factors can make it more likely to develop
tendinitis, including:

A bone spur that has developed where the

tendon attaches to the heel bone.

Sudden increase in the amount or

intensity of exercise activityfor
example, increasing the distance
you run every day by a few miles
without giving your body a chance
to adjust to the new distance

Tight calf musclesHaving tight

calf muscles and suddenly starting
 an aggressive exercise program
can put extra stress on the Achilles
tendon

Bone spurExtra bone growth

where the Achilles tendon attaches
to the heel bone can rub against
the tendon and cause pain

Top of page
Symptoms
Common symptoms of Achilles tendinitis
include:

Pain and stiffness along the Achilles

tendon in the morning

Pain along the tendon or back of

the heel that worsens with activity

Severe pain the day after

exercising

Thickening of the tendon

Bone spur (insertional tendinitis)

Swelling that is present all the time

and gets worse throughout the day
with activity

If you have experienced a sudden "pop" in

the back of your calf or heel, you may
have ruptured (torn) your Achilles tendon.
See your doctor immediately if you think
you may have torn your tendon.
Top of page
Doctor Examination
After you describe your symptoms and
discuss your concerns, the doctor will
examine your foot and ankle. The doctor
will look for these signs:
 Swelling along the Achilles tendon
or at the back of your heel

Thickening or enlargement of the

Achilles tendon

Bony spurs at the lower part of the

tendon at the back of your heel
(insertional tendinitis)

The point of maximum tenderness

Pain in the middle of the tendon,

(noninsertional tendinitis)

Pain at the back of your heel at the

lower part of the tendon
(insertional tendinitis)

Limited range of motion in your

anklespecifically, a decreased
ability to flex your foot

Testsr doctor may order imaging tests to

make sure your symptoms are caused by
Achilles tendinitis.

X-rays
X-ray tests provide clear images of bones.
X-rays can show whether the lower part of
the Achilles tendon has calcified, or
become hardened. This calcification
indicates insertional Achilles tendinitis. In
cases of severe noninsertional Achilles
tendinitis, there can be calcification in the
middle portion of the tendon, as well.

Magnetic Resonance Imaging (MRI)

Although magnetic resonance imaging
(MRI) is not necessary to diagnose
Achilles tendinitis, it is important for
planning surgery. An MRI scan can show
how severe the damage is in the tendon.
If surgery is needed, your doctor will
select the procedure based on the amount
of tendon damage.
Top of page
Treatment

Nonsurgical Treatment
In most cases, nonsurgical treatment
options will provide pain relief, although it
may take a few months for symptoms to
completely subside. Even with early
treatment, the pain may last longer than
3 months. If you have had pain for several
months before seeking treatment, it may
take 6 months before treatment methods
take effect.
Rest. The first step in reducing pain is to
decrease or even stop the activities that
make the pain worse. If you regularly do
high-impact exercises (such as running),
switching to low-impact activities will put
less stress on the Achilles tendon. Cross-
training activities such as biking, elliptical
exercise, and swimming are low-impact
options to help you stay active.
Ice. Placing ice on the most painful area of
the Achilles tendon is helpful and can be
done as needed throughout the day. This
can be done for up to 20 minutes and
should be stopped earlier if the skin
becomes numb. A foam cup filled with
water and then frozen creates a simple,
reusable ice pack. After the water has
frozen in the cup, tear off the rim of the
cup. Then rub the ice on the Achilles
tendon. With repeated use, a groove that
fits the Achilles tendon will appear,
creating a "custom-fit" ice pack.
Non-steroidal anti-inflammatory
medication. Drugs such as ibuprofen and
naproxen reduce pain and swelling. They
do not, however, reduce the thickening of
the degenerated tendon. Using the
medication for more than 1 month should
be reviewed with your primary care
doctor.
Exercise. The following exercise can help
to strengthen the calf muscles and reduce
stress on the Achilles tendon.

Calf stretch
Lean forward against a wall with
one knee straight and the heel on
the ground. Place the other leg in
front, with the knee bent. To stretch
the calf muscles and the heel cord,
push your hips toward the wall in a
controlled fashion. Hold the position
for 10 seconds and relax. Repeat
this exercise 20 times for each foot.
A strong pull in the calf should be
felt during the stretch.

Physical Therapy. Physical therapy is very

helpful in treating Achilles tendinitis. It
has proven to work better for
noninsertional tendinitis than for
insertional tendinitis.
Eccentric Strengthening Protocol.
Eccentric strengthening is defined as
contracting (tightening) a muscle while it
is getting longer. Eccentric strengthening
exercises can cause damage to the
Achilles tendon if they are not done
correctly. At first, they should be
performed under the supervision of a
physical therapist. Once mastered with a
therapist, the exercises can then be done
at home. These exercises may cause
some discomfort, however, it should not
be unbearable.

Bilateral heel drop

Stand at the edge of a stair, or a
raised platform that is stable, with
just the front half of your foot on
the stair. This position will allow
your heel to move up and down
without hitting the stair. Care must
be taken to ensure that you are
balanced correctly to prevent
falling and injury. Be sure to hold
onto a railing to help you balance.

Lift your heels off the ground then

slowly lower your heels to the
lowest point possible. Repeat this
step 20 times. This exercise should
be done in a slow, controlled
fashion. Rapid movement can
create the risk of damage to the
tendon. As the pain improves, you
can increase the difficulty level of
the exercise by holding a small
weight in each hand.

Single leg heel drop

This exercise is performed similarly
to the bilateral heel drop, except
that all your weight is focused on
one leg. This should be done only
after the bilateral heel drop has
been mastered.

Cortisone injections. Cortisone, a type of

steroid, is a powerful anti-inflammatory
medication. Cortisone injections into the
Achilles tendon are rarely recommended
because they can cause the tendon to
rupture (tear).
Supportive shoes and orthotics. Pain from
insertional Achilles tendinitis is often
helped by certain shoes, as well as
orthotic devices. For example, shoes that
are softer at the back of the heel can
reduce irritation of the tendon. In
addition, heel lifts can take some strain
off the tendon.
Heel lifts are also very helpful for patients
with insertional tendinitis because they
can move the heel away from the back of
the shoe, where rubbing can occur. They
also take some strain off the tendon. Like
a heel lift, a silicone Achilles sleeve can
reduce irritation from the back of a shoe.
If your pain is severe, your doctor may
recommend a walking boot for a short
time. This gives the tendon a chance to
rest before any therapy is begun.
Extended use of a boot is discouraged,
though, because it can weaken your calf
muscle.
Extracorporeal shockwave therapy
(ESWT). During this procedure, high-
energy shockwave impulses stimulate the
healing process in damaged tendon
tissue. ESWT has not shown consistent
results and, therefore, is not commonly
performed.
ESWT is noninvasiveit does not require
a surgical incision. Because of the
minimal risk involved, ESWT is sometimes
tried before surgery is considered.

Surgical Treatment
Surgery should be considered to relieve
Achilles tendinitis only if the pain does not
improve after 6 months of nonsurgical
treatment. The specific type of surgery
depends on the location of the tendinitis
and the amount of damage to the tendon.
Gastrocnemius recession. This is a
surgical lengthening of the calf
(gastrocnemius) muscles. Because tight
calf muscles place increased stress on the
Achilles tendon, this procedure is useful
for patients who still have difficulty flexing
their feet, despite consistent stretching.
In gastrocnemius recession, one of the
two muscles that make up the calf is
lengthened to increase the motion of the
ankle. The procedure can be performed
with a traditional, open incision or with a
smaller incision and an endoscopean
instrument that contains a small camera.
Your doctor will discuss the procedure that
best meets your needs.
Complication rates for gastrocnemius
recession are low, but can include nerve
damage.
Gastrocnemius recession can be
performed with or without dbridement,
which is removal of damaged tissue.
Dbridement and repair (tendon has less
than 50% damage). The goal of this
operation is to remove the damaged part
of the Achilles tendon. Once the
unhealthy portion of the tendon has been
removed, the remaining tendon is
repaired with sutures, or stitches to
complete the repair.
In insertional tendinitis, the bone spur is
also removed. Repair of the tendon in
these instances may require the use of
metal or plastic anchors to help hold the
Achilles tendon to the heel bone, where it
attaches.
After dbridement and repair, most
patients are allowed to walk in a
removable boot or cast within 2 weeks,
although this period depends upon the
amount of damage to the tendon.
Dbridement with tendon transfer
(tendon has greater than 50% damage).
In cases where more than 50% of the
Achilles tendon is not healthy and
requires removal, the remaining portion of
the tendon is not strong enough to
function alone. To prevent the remaining
tendon from rupturing with activity, an
Achilles tendon transfer is performed. The
tendon that helps the big toe point down
is moved to the heel bone to add strength
to the damaged tendon. Although this
sounds severe, the big toe will still be able
to move, and most patients will not notice
a change in the way they walk or run.
Depending on the extent of damage to
the tendon, some patients may not be
able to return to competitive sports or
running.
Recovery. Most patients have good results
from surgery. The main factor in surgical
recovery is the amount of damage to the
tendon. The greater the amount of tendon
involved, the longer the recovery period,
and the less likely a patient will be able to
return to sports activity.
Physical therapy is an important part of
recovery. Many patients require 12
months of rehabilitation before they are
pain-free.
Complications. Moderate to severe pain
after surgery is noted in 20% to 30% of
patients and is the most common
complication. In addition, a wound
infection can occur and the infection is
very difficult to treat in this location.

2)HAGLUNDS DEFORMITY:
Haglund's deformity (also referred to as
Mulholland deformity, retrocalcaneal
bursitis, posterior calcaneal
tuberosity, and pump bump) is a bony
enlargement on the back of the heel that
most often leads to painful bursitis, which
is an inflammation of the bursa (a fluid-
filled sac between the tendon and bone).
In Haglund's deformity, the soft tissue
near the Achilles tendon becomes irritated
when the bony enlargement rubs against
shoes.
Haglund's deformity is often called "pump
bump" because the rigid backs of pump-
style shoes can create pressure that
aggravates the enlargement when
walking.

Symptoms
Haglund's deformity can occur in one or
both feet. The signs and symptoms
include:

A noticeable bump on the back of

heel.

Pain in the area where the Achilles

tendon attaches to the heel.

Swelling in the back of the heel.

Redness near the inflamed tissue.

Causes
To some extent, heredity plays a role in
Haglund's deformity. People can inherit a
type of foot structure that makes them
prone to developing this condition.
For example, high arches can contribute
to Haglund's deformity. The Achilles
tendon attaches to the back of the heel
bone, and in a person with high arches,
the heel bone is tilted backward into the
Achilles tendon. This causes the
uppermost portion of the back of the heel
bone to rub against the tendon.
Eventually, due to this constant irritation,
a bony protrusion develops and the bursa
becomes inflamed. It is the inflamed
bursa that produces the redness and
swelling associated with Haglund's
deformity.
A tight Achilles tendon can also play a role
in Haglund's deformity, causing pain by
compressing the tender and inflamed
bursa. In contrast, a tendon that is more
flexible results in less pressure against the
painful bursa.
Another possible contributor to Haglund's
deformity is a tendency to walk on the
outside of the heel. This tendency, which
produces wear on the outer edge of the
sole of the shoe, causes the heel to rotate
inward, resulting in a grinding of the heel
bone against the tendon. The tendon
protects itself by forming a bursa, which
eventually becomes inflamed and tender.

Diagnosis
After evaluating the patient's symptoms,
the foot and ankle surgeon will examine
the foot. In addition, x-rays will be
requested to help the surgeon evaluate
the structure of the heel bone.

Haglund's deformity in ankle

Treatment
Non-surgical treatment of Haglund's
deformity is aimed at reducing the
inflammation of the bursa. While these
approaches can resolve the bursitis, they
will not shrink the bony protrusion. Non-
surgical treatment can include one or
more of the following:

Removal of the problem: Walking

without shoes takes the pressure
completely off the affected area.
 Medication. Anti-inflammatory
medications may help reduce the
pain and inflammation. Some
patients also find that a topical pain
reliever, which is applied directly to
the inflamed area, is beneficial.

Ice. To reduce swelling, apply a bag

of ice over a thin towel to the
affected area for 20 minutes of
each waking hour. Do not put ice
directly against the skin.

Exercises. Stretching exercises help

relieve tension from the Achilles
tendon. These exercises are
especially important for the patient
who has a tight heel cord.

Heel lifts. Patients with high arches

may find that heel lifts placed
inside the shoe decrease the
pressure on the heel.

Shoe modification. Wearing shoes

that are backless or have soft backs
will avoid or minimize irritation.

Physical therapy. A physical

therapist can help identify
biomechanical abnormalities that
may be contributing to
inflammation and recommend
appropriate strengthening and
stretching exercises to help
decrease discomfort and prevent
the need for surgery.

Orthotic devices. These custom

arch supports are helpful because
they control the motion in the foot,
which can aggravate symptoms.
 Immobilization. In some cases,
casting may be necessary to
reduce symptoms.

If non-surgical treatment fails to provide

adequate pain relief, surgery may be
needed consisting of debridement of the
affected Achilles tendon and excision of
the retrocalcaneal bursa and the Haglund
deformity. A central approach facilitates
such debridement but necessitates
detachment of 50% of the Achilles tendon
from the calcaneus which is usually
sutured back using bone anchors. In
severe cases necessitating debridement
of a substantial portion of the Achilles
tendon, augmentation may be done with
the transfer of the flexor hallucis longus
muscle.

Prevention
A recurrence of Haglund's deformity may
be prevented by:

Wearing appropriate shoes; avoid

pumps and high-heeled shoes.

Using arch supports or orthotic

devices.

Performing stretching exercises to

prevent the Achilles tendon from
tightening.

Avoiding running on hard surfaces

and running uphill.

3)PLANTAR FASCITIS:
Plantar fasciitis is a disorder that results
in pain in the heel and bottom of the foot.
[1]
The pain is usually most severe with the
first steps of the day or following a period
of rest.[2] Pain is also frequently brought
on by bending the foot and toes up
towards the shin and may be worsened by
a tight Achilles tendon.[2][3] The condition
typically comes on slowly.[3] In about a
third of people both legs are affected.[1]
The causes of plantar fasciitis are not
entirely clear. Risk factors include overuse
such as from long periods of standing, an
increase in exercise, and obesity.[1] It is
also associated with inward rolling of the
foot and a lifestyle that involves little
exercise.[1][2] While heel spurs are
frequently found it is unclear if they have
a role in causing the condition. Plantar
fasciitis is a disorder of the insertion site
of the ligament on the bone characterized
by micro tears, breakdown of collagen,
and scarring.[1] As inflammation plays a
lesser role, many feel the condition should
be renamed plantar fasciosis.[1][4] The
diagnosis is typically based on signs and
symptoms with ultrasound sometimes
used to help.[1] Other conditions with
similar symptoms include osteoarthritis,
ankylosing spondylitis, heel pad
syndrome, and reactive arthritis.

Signs and symptoms

When plantar fasciitis occurs, the pain is
typically sharp[9] and usually unilateral
(70% of cases).[7] Heel pain is worsened
by bearing weight on the heel after long
periods of rest.[10] Individuals with plantar
fasciitis often report their symptoms are
most intense during their first steps after
getting out of bed or after prolonged
periods of sitting.[2] Improvement of
symptoms is usually seen with continued
walking.[2][6][9] Rare, but reported
symptoms include numbness, tingling,
swelling, or radiating pain.[11] Typically
there are no fevers or night sweats.[3]
If the plantar fascia continues to be
overused in the setting of plantar fasciitis,
the plantar fascia can rupture. Typical
signs and symptoms of plantar fascia
rupture include a clicking or snapping
sound, significant local swelling, and
acute pain in the sole of the foot. [9]

Risk factors
Identified risk factors for plantar fasciitis
include excessive running, standing on
hard surfaces for prolonged periods of
time, high arches of the feet, the
presence of a leg length inequality, and
flat feet. The tendency of flat feet to
excessively roll inward during walking or
running makes them more susceptible to
plantar fasciitis.[2][10][12] Obesity is seen in
70% of individuals who present with
plantar fasciitis and is an independent risk
factor.[3] Studies have suggested a strong
association exists between an increased
body mass index and the development of
plantar fasciitis in the non-athletic
population; this association between
weight and plantar fasciitis has not been
observed in the athletic population.[7]
Achilles tendon tightness and
inappropriate footwear have also been
identified as significant risk factors. [13]

Pathophysiology

Drawing of the plantar fascia of the foot

The cause of plantar fasciitis is poorly
understood and is thought to likely have
several contributing factors.[13] The
plantar fascia is a thick fibrous band of
connective tissue that originates from the
medial tubercle and anterior aspect of the
heel bone. From there, the fascia extends
along the sole of the foot before inserting
at the base of the toes, and supports the
arch of the foot.[3][10][12]
Originally, plantar fasciitis was believed to
be an inflammatory condition of the
plantar fascia. However, within the last
decade, studies have observed
microscopic anatomical changes
indicating that plantar fasciitis is actually
due to a noninflammatory structural
breakdown of the plantar fascia rather
than an inflammatory process.[7][13]
Due to this shift in thought about the
underlying mechanisms in plantar
fasciitis, many in the academic
community have stated the condition
should be renamed plantar fasciosis. [6]
The structural breakdown of the plantar
fascia is believed to be the result of
repetitive microtrauma (small tears).[11][12]
Microscopic examination of the plantar
fascia often shows myxomatous
degeneration, connective tissue calcium
deposits, and disorganized collagen
fibers.[4]
Disruptions in the plantar fascia's normal
mechanical movement during standing
and walking (known as the Windlass
mechanism) are thought to contribute to
the development of plantar fasciitis by
placing excess strain on the calcaneal
tuberosity.[13] Other studies have also
suggested that plantar fasciitis is not
actually due to inflamed plantar fascia,
but may be a tendon injury involving the
flexor digitorum brevis muscle located
immediately deep to the plantar fascia.[12]
Diagnosis

Achilles tendon tightness is a risk factor

for plantar fasciitis. It can lead to
decreased dorsiflexion of the foot.

Heel bone with heel spur (red arrow)

Thickened plantar fascia in ultrasound

Plantar fasciitis is usually diagnosed by a
health care provider after consideration of
a person's presenting history, risk factors,
and clinical examination.[2][14][15]
Tenderness to palpation along the inner
aspect of the heel bone on the sole of the
foot may be elicited during the physical
examination.[2][10] The foot may have
limited dorsiflexion due to tightness of the
calf muscles or the Achilles tendon.[7]
Dorsiflexion of the foot may elicit the pain
due to stretching of the plantar fascia
with this motion.[2][11] Diagnostic imaging
studies are not usually needed to
diagnose plantar fasciitis.[7] However, in
certain cases a physician may decide
imaging studies (such as X-rays,
diagnostic ultrasound or MRI) are
warranted to rule out serious causes of
foot pain.
Other diagnoses that are typically
considered include fractures, tumors, or
systemic disease if plantar fasciitis pain
fails to respond appropriately to
conservative medical treatments.[2][10]
Bilateral heel pain or heel pain in the
context of a systemic illness may indicate
a need for a more in-depth diagnostic
investigation. Diagnostic tests such as a
CBC or serological markers of
inflammation, infection, or autoimmune
disease such as C-reactive protein,
erythrocyte sedimentation rate, anti-
nuclear antibodies, rheumatoid factor,
HLA-B27, uric acid, or Lyme disease
antibodies may also be obtaine

Treatment
Non-surgical
About 90% of plantar fasciitis cases will
improve within six months with
conservative treatment,[8] and within a
year regardless of treatment.[2][7] Many
treatments have been proposed for
plantar fasciitis. Most have not been
adequately investigated and there is little
evidence to support recommendations for
such treatments.[2] First-line conservative
approaches include rest, heat, ice, and
calf-strengthening exercises; techniques
to stretch the calf muscles, Achilles
tendon, and plantar fascia; weight
reduction in the overweight or obese; and
nonsteroidal anti-inflammatory drugs
(NSAIDs) such as aspirin or ibuprofen.[6][10]
[20]
NSAIDs are commonly used to treat
plantar fasciitis, but fail to resolve the
pain in 20% of people.[10]
Extracorporeal shockwave therapy (ESWT)
is an effective treatment modality for
plantar fasciitis pain unresponsive to
conservative nonsurgical measures for at
least three months. Evidence from meta-
analyses suggests significant pain relief
lasts up to one year after the procedure.[8]
[21]
However, debate about the therapy's
efficacy has persisted.[4] ESWT can be
performed with or without anesthesia
though studies have suggested that the
therapy is less effective when anesthesia
is given.[22] Complications from ESWT are
rare and typically mild when present.[22]
Known complications of ESWT include the
development of a mild hematoma or an
ecchymosis, redness around the site of
the procedure, or migraine.[22]
Corticosteroid injections are sometimes
used for cases of plantar fasciitis
refractory to more conservative
measures. The injections may be an
effective modality for short-term pain
relief up to one month, but studies failed
to show effective pain relief after three
months.[4] Notable risks of corticosteroid
injections for plantar fasciitis include
plantar fascia rupture,[3] skin infection,
nerve or muscle injury, or atrophy of the
plantar fat pad.[2][10] Custom orthotic
devices have been demonstrated as an
effective method to reduce plantar
fasciitis pain for up to 12 weeks.[23] The
long-term effectiveness of custom
orthotics for plantar fasciitis pain
reduction requires additional study. [24]
Orthotic devices and certain taping
techniques are proposed to reduce
pronation of the foot and therefore reduce
load on the plantar fascia resulting in pain
improvement.[12]
Another treatment technique known as
plantar iontophoresis involves applying
anti-inflammatory substances such as
dexamethasone or acetic acid topically to
the foot and transmitting these
substances through the skin with an
electric current.[10] Moderate evidence
exists to support the use of night splints
for 13 months to relieve plantar fasciitis
pain that has persisted for six months. [7]
The night splints are designed to position
and maintain the ankle in a neutral
position thereby passively stretching the
calf and plantar fascia overnight during
sleep.[7] Other treatment approaches may
include supportive footwear, arch taping,
and physical therapy.[6]
Surgery
Plantar fasciotomy is often considered
after conservative treatment has failed to
resolve the issue after six months and is
viewed as a last resort.[2][6] Minimally
invasive and endoscopic approaches to
plantar fasciotomy exist but require a
specialist who is familiar with certain
equipment. The availability of these
surgical techniques is currently limited.[5]
A 2012 study found 76% of patients who
underwent endoscopic plantar fasciotomy
had complete relief of their symptoms
and had few complications (level IV
evidence).[4] Heel spur removal during
plantar fasciotomy has not been found to
improve the surgical outcome.[25] Plantar
heel pain may occur for multiple reasons
and release of the lateral plantar nerve
branch may be performed alongside the
plantar fasciotomy in select cases.[5][25]
Possible complications of plantar
fasciotomy include nerve injury, instability
of the medial longitudinal arch of the foot,
[26]
fracture of the calcaneus, prolonged
recovery time, infection, rupture of the
plantar fascia, and failure to improve the
pain.[2] Coblation surgery has recently
been proposed as alternative surgical
approaches for the treatment of
recalcitrant plantar fasciitis
2) A calcaneal spur (or heel spur) is a
small osteophyte (bone spur) located on
the calcaneus (heel bone). Calcaneal
spurs are typically detected by a
radiographic examination (commonly
referred to as an "x-ray").
When a foot bone is exposed to constant
stress, calcium deposits build up on the
bottom of the heel bone. Generally, this
has no effect on a person's daily life.
However, repeated damage can cause
these deposits to pile up on each other,
causing a spur-shaped deformity, called a
calcaneal (or heel) spur. Obese people,
flatfooted people, and people who often
wear high-heeled shoes are most
susceptible to heel spurs.
An inferior calcaneal spur is located on
the inferior aspect of the calcaneus and is
typically a response to plantar fasciitis
over a period, but may also be associated
with ankylosing spondylitis (typically in
children). A posterior calcaneal spur
develops on the back of the heel at the
insertion of the Achilles tendon.
An inferior calcaneal spur consists of a
calcification of the calcaneus, which lies
superior to the plantar fascia at the
insertion of the plantar fascia. A posterior
calcaneal spur is often large and palpable
through the skin and may need to be
removed as part of the treatment of
insertional Achilles tendonitis.[1] These are
also generally visible to the naked eye.[2]
Signs and symptoms

Inferior calcaneal spur

Major symptoms consist of pain in the
region surrounding the spur, which
typically increases in intensity after
prolonged periods of rest. Patients may
report heel pain to be more severe when
waking up in the morning. Patients may
not be able to bear weight on the afflicted
heel comfortably. Running, walking, or
lifting heavy weight may exacerbate the
issue.

Treatment
Many treatment options exist, and good
results are often observed. Generally, a
calcaneal spur develops when proper care
is not given to the foot and heels. It is
often seen as a repetitive stress injury,
and thus lifestyle modification is typically
the basic course of management
strategies.
To alleviate heel spur pain, a person
should begin doing foot and calf workouts.
Strong muscles in the calves and lower
legs will help take the stress off the bone
and thus help cure or prevent heel spurs.
Icing the area is an effective way to get
immediate pain relief
[D]JOINT DISORDERS: ;
1) A bunion is a deformity of the joint
connecting the big toe to the foot. It is
characterized by medial deviation[further
explanation needed][disambiguation needed]
of the first
metatarsal bone and lateral deviation[further
explanation needed]
of the hallux (big toe), often
erroneously described as an enlargement
of bone or tissue around the joint at the
bottom of the big toe (known as the
metatarsophalangeal joint).
There is disagreement among medical
professionals about the cause of bunions.
Some see them as primarily caused by
the long-term use of shoes, particularly
tight-fitting shoes with pointed toes.[1]
Others believe that the problem stems
from genetic factors that are exacerbated
by shoe use.[2] Bunions occur when
pressure is applied to the side of the big
toe (hallux) forcing it inwards towards,
and sometimes under or over, the other
toes (angulation). As pressure is applied,
the tissues surrounding the joint may
become swollen and tender. In a survey of
people from cultures that do not wear
shoes, no cases of bunions were found,
lending credence to the hypothesis that
bunions are caused by ill-fitting shoes.[3]
The bump itself is partly due to the
swollen bursal sac or an osseous (bony)
anomaly on the metatarsophalangeal
joint. The larger part of the bump is a
normal part of the head of the first
metatarsal bone that has tilted sideways
to stick out at its distal (far) end.

Signs and symptoms

Illustration depicting a bunion

The symptoms of bunions include irritated
skin around the bunion, pain when
walking, joint redness and pain, and
possible shift of the big toe toward the
other toes. Blisters may form more easily
around the site of the bunion as well.
Having bunions can also make it difficult
to find shoes that fit properly and bunions
may force a person to have to buy a
larger size shoe to accommodate the
width the bunion creates. When bunion
deformity becomes severe enough, the
foot can hurt in different places even
without the constriction of shoes because
it then becomes a mechanical function
problem of the forefoot.

Pathophysiology
Bunions are sometimes genetic[dubious discuss]
and consist of certain tendons, ligaments,
and supportive structures of the first
metatarsal that are positioned differently.
This bio-mechanical anomaly may be
caused by a variety of conditions intrinsic
to the structure of the foot such as flat
feet, excessive flexibility of ligaments,
abnormal bone structure, and certain
neurological conditions. These factors are
often considered genetic. Although some
experts are convinced that poor-fitting
footwear is the main cause of bunion
formation,[4] other sources concede that
footwear only exacerbates the problem
caused by the original genetic structure. [2]
Bunions are commonly associated with a
deviated position of the big toe toward
the second toe, and the deviation in the
angle between the first and second
metatarsal bones of the foot. The small
sesamoid bones found beneath the first
metatarsal (which help the flexor tendon
bend the big toe downwards) may also
become deviated over time as the first
metatarsal bone drifts away from its
normal position. Arthritis of the big toe
joint, diminished and/or altered range of
motion, and discomfort with pressure
applied to the bump or with motion of the
joint, may all accompany bunion
development. Atop of the first metatarsal
head either medially or dorso-medially,
there can also arise a bursa that when
inflamed (bursitis), can be the most
painful aspect of the process.

Diagnosis

X-ray showing measurements of HVA and

IMA angles of hallux valgus.
Bunion can be diagnosed and analyzed by
plain projectional radiography. The hallux
valgus angle (HVA) is the angle between
the longitudinal axes of the proximal
phalanx and the first metatarsal bone of
the big toe. It is considered abnormal if
greater than 15-18 degrees.[5] The
intermetatarsal angle (IMA) is the angle
between the longitudinal axes of the first
and second metatarsal bones, and is
normally less than 9 degrees.[5]

Treatment
Bunions may be treated conservatively
with changes in footwear, the use of
orthotics (accommodative padding and
shielding), rest, ice and medications.
These sorts of treatments address
symptoms more than they correct the
actual deformity. Surgery, by an
orthopedic surgeon or a podiatric
surgeon, may be necessary if discomfort
is severe enough or when correction of
the deformity is desired.
Orthotics
Orthotics are splints or regulators while
conservative measures include various
footwear like gelled toe spacers, bunion /
toes separators, bunion regulators, bunion
splints and bunion cushions. There are a
variety of available orthotics (or orthoses)
including over-the-counter or off-the-shelf
commercial products and as necessary,
custom-molded orthotics that are
generally prescribed medical devices.
Surgery
A podiatric surgeon performing surgery to
remove the bony enlargement and restore
normal alignment of the toe joint.

Bunionectomy
Procedures are designed and chosen to
correct a variety of pathologies that may
be associated with the bunion. For
instance, procedures may address some
combination of:

removing the abnormal bony

enlargement of the first metatarsal,

realigning the first metatarsal bone

relative to the adjacent metatarsal
bone,

straightening the great toe relative

to the first metatarsal and adjacent
toes,

realigning the cartilagenous

surfaces of the great toe joint,

addressing arthritic changes

associated with the great toe joint,

repositioning the sesamoid bones

beneath the first metatarsal bone,

shortening, lengthening, raising, or

lowering the first metatarsal bone,
and

correcting any abnormal bowing or

misalignment within the great toe.
 Connecting two parallel long bones
side by side by Syndesmosis
Procedure

2)CUBOID SYNDROME:
Cuboid syndrome or cuboid
subluxation describes a condition that
results from subtle injury to the
calcaneocuboid joint[1] and ligaments in
the vicinity of the cuboid bone, one of
seven tarsal bones of the human foot.
This condition often manifests in the form
of lateral (little toe side) foot pain and
sometimes general foot weakness. Cuboid
syndrome, which is relatively common but
not well defined or recognized,[2] is known
by many other names, including "lateral
plantar neuritis, cuboid fault syndrome,
peroneal cuboid syndrome, dropped
cuboid, locked cuboid and subluxed
cuboid.[1][3]

Signs and symptoms

A patient with cuboid syndrome usually
seeks medical advice and attention
complaining of pain, discomfort, or
weakness along the lateral aspect of the
foot between the fourth and fifth
metatarsals and the calcaneocuboid joint.
[1]
The pain may radiate throughout the
foot.[1] Tenderness may be elicited over
the tendon of the peroneus longus muscle
and an antalgic gait may be observed.[1]
The pain may be observed in a controlled
environment by standing on the toes or
rolling the arches of the foot, as these
motions tend to exercise the foot's
calcaneocuboid joint and ligament, which
are characteristically strained in a patient
suffering from cuboid syndrome.[4] Also,
the pain may come on suddenly or it may
develop gradually and persist over time.
Sometimes the pain is intermittent,
subsiding partially or completely for a
period of time before returning again.[3]

Causes
A patient may develop Cuboid syndrome
through either a single traumatic event
(e.g., ankle sprain) or insidiously with
repetitive strain over time.[1] The exact
etiology of Cuboid syndrome remains
unclear but many ideas have been
proposed. Such ideas include excessive
pronation of the foot, overuse injury, and
inversion ankle sprains.[1] The favored
idea is that the cuboid bone is forcefully
everted while the calcaneus is inverted
resulting in incongruity at the
calcaneocuboid joint.[1] The condition
mainly affects athletes, especially those
whose activities incur a significant
amount of pressure on their feet from
jumping or running (such as ballet
dancers[5] and runners) and those who
place added strain on their feet during
lateral maneuvering (such as tennis and
basketball players[3][4]). Cuboid syndrome
may persist even if the patient is taking
part in regular physical therapy.[3] The
patient's foot type, such as the presence
of overpronation or underpronation, may
also play a factor in the condition.

Risk factors
Suspected risk factors for Cuboid
syndrome include obesity, midtarsal
instability, poorly fitting footwear,
physical exercise, inadequate recovery
from physical activity, physical training on
uneven surfaces, and ankle sprains.[1]

Treatment
Once diagnosed, a medical professional
may treat cuboid syndrome by realigning
(also known as reducing) the subluxed
cuboid unless contraindications to
manipulation are present such as gout,
inflammatory arthritis, bony disease,
neurovascular compromise, or a bone
fracture.[1][3] This form of manual
manipulation of the foot should be done
by a trained specialist, such as a
podiatrist, chiropractor, osteopath,
athletic trainer, osteopathic physician, or
physical therapist. Further treatment may
take into account other considerations,
such as possible causes or aggravators
(e.g. recommending that the patient be fit
with custom orthotics if they are
overprone). Fortunately, subluxed cuboids
are generally quite treatable[4] and most
patients return to a normal level of
activity once the pain is brought under
controL
3)HALLUS RIGIDUS:
Hallux rigidus or stiff big toe is
degenerative arthritis and stiffness due to
bone spurs that affects the MTP joint at
the base of the hallux (big toe).
Hallux flexus was initially described by
Davies-Colley[1] in 1887 as a plantar flexed
posture of phalanx relative to the
metatarsal head. About the same time,
Cotterill first used the term hallux rigidus.

Causes
This condition, which occurs in
adolescents and adults, can be associated
with previous trauma. The true cause is
not known. Most commonly, hallux rigidus
is thought to be caused by wear and tear
of the first metatarsophalangeal joint.

Symptoms

Pain and stiffness in the joint at the

base of the big toe during use
(walking, standing, bending, etc.)
 Difficulty with certain activities
(running, squatting)

Swelling and inflammation around

the joint

Although the condition is degenerative, it

can occur in patients who are relatively
young particularly active sports people
who have at some time suffered trauma
to the joint (turf toe). A notable example
is NBA star Shaquille O'Neal[2] who
returned to basketball after surgery.

Classification
In 1988, Hattrup and Johnson described
the following radiographic classification
system: Grade I - mild changes with
maintained joint space and minimal
spurring. Grade II - moderate changes
with narrowing of joint space, bony
proliferation on the metatarsophalangeal
head and phalanx and subchondral
sclerosis or cyst. Grade III - Severe
changes with significant joint space
narrowing, extensive bony proliferation
and loose bodies or a dorsal ossicle.[3]

Treatment
Non-surgical treatment Early treatment
for mild cases of hallux rigidus may
include prescription foot orthotics, shoe
modifications (to take the pressure off the
toe and/or facilitate walking), medications
(anti-inflammatory drugs), injection
therapy (corticosteroids to reduce
inflammation and pain) and/or physical
therapy.
Surgical treatment In some cases,
surgery is the only way to eliminate or
reduce pain. There are several types of
surgery for treatment of hallux rigidus.
The type of surgery is based on the stage
of hallux rigidus. Stage 1 hallux rigidus
involves some loss of range of motion of
the big toe joint or first MTP joint and is
often treated conservatively with
prescription foot orthotics. Stage 2 hallux
rigidus involves greater loss of range of
motion and cartilage and may be treated
via cheilectomy in which the metatarsal
head is reshaped and bone spurs reduced.
Stage 3 hallux rigidus often involves
significant cartilage loss and may be
treated by an osteotomy in which
cartilage on the first metatarsal head is
repositioned, possibly coupled with a
hemi-implant in which the base of the
proximal phalanx (base of the big toe) is
resurfaced. Stage 4 hallux rigidus, also
known as end stage hallux rigidus
involves severe loss of range of motion of
the big toe joint and cartilage loss. Stage
4 hallux rigidus may be treated via fusion
of the joint (arthrodesis) or implant
arthroplasty in which both sides of the
joint are resurfaced or a hinged implant is
used. Fusion of the joint is often viewed as
more definitive but may lead to significant
alteration of gait causing postural
symptomatology. The implants termed
"two part unconstrained" implants in
which a "ball" type device is placed on the
first metatarsal head and "socket" portion
on the base of the big toe do not have a
good long term track record. The hinged
implants have been in existence since the
1970s, have been continually improved
and have the best record of improving
long term function.
4)TAILORS BUNION: Tailor's bunion, or
bunionette, is a condition caused as a
result of inflammation of the fifth
metatarsal bone at the base of the little
toe.[1]
It is mostly similar to a bunion (the same
type of ailment affecting the big toe). It is
called Tailor's Bunion because in past
centuries, tailors sat cross-legged,[2] and
this was thought to cause this protrusion
on the outside aspect of the foot.
It is usually characterized by
inflammation, pain and redness of the
little toe.
Often a tailor's bunion is caused by a
faulty mechanical structure of the foot.
The fifth metatarsal bone starts to
protrude outward, while the little toe
moves inward. This change in alignment
creates an enlargement on the outside of
the foot.
Tailor's bunion is easily diagnosed
because the protrusion is visually
apparent. X-rays may be ordered to help
the surgeon find out the severity of the
deformity.

Treatment
Non-surgical therapies include:[1]

Shoe modifications: wearing shoes

that have a wide toe box, and
avoiding those with pointed toes or
high heels.

Oral nonsteroidal anti-inflammatory

drugs may help in relieving the
pain and inflammation.

Injections of corticosteroid are

commonly used to treat the
inflammation.

Bunionette pads placed over the

affected area may help reduce
pain.

An ice pack may be applied to

reduce pain and inflammation.

Surgery is often considered when pain

continues for a long period with no
improvement in these non-surgical
therapies

[E]NERVE DISORDERS:
1) MORTAN,S NEUROMA:
Morton's neuroma (also known as
Morton neuroma, Morton's
metatarsalgia, Intermetatarsal
neuroma and Intermetatarsal space
neuroma.[1]) is a benign neuroma of an
intermetatarsal plantar nerve, most
commonly of the second and third
intermetatarsal spaces (between 2nd3rd
and 3rd4th metatarsal heads), which
results in the entrapment of the affected
nerve. The main symptoms are pain
and/or numbness, sometimes relieved by
removing narrow or high-heeled footwear.
Sometimes symptoms are relieved by
wearing non-constricting footwear.
Some sources claim that entrapment of
the plantar nerve because of compression
between the metatarsal heads, as
originally proposed by Morton, is highly
unlikely, because the plantar nerve is on
the plantar side of the transverse
metatarsal ligament and thus does not
come in contact with the metatarsal
heads. It is more likely that the transverse
metatarsal ligament is the cause of the
entrapment.[2][3]
Despite the name, the condition was first
correctly described by a chiropodist
named Durlacher,[4] and although it is
labeled a "neuroma", many sources do
not consider it a true tumor, but rather a
perineural fibroma (fibrous tissue
formation around nerve tissue).

Symptoms and signs

Symptoms include: pain on weight
bearing, frequently after only a short
time. The nature of the pain varies widely
among individuals. Some people
experience shooting pain affecting the
contiguous halves of two toes. Others
describe a feeling like having a pebble in
their shoe or walking on razor blades.
Burning, numbness, and paresthesia may
also be experienced.[5] The symptoms
progress over time, often beginning as a
tingling sensation in the ball of the foot. [6]
Morton's neuroma lesions have been
found using MRI in patients without
symptoms.[7]

Diagnosis/differential diagnosis
Negative signs include no obvious
deformities, erythema, signs of
inflammation, or limitation of movement.
Direct pressure between the metatarsal
heads will replicate the symptoms, as will
compression of the forefoot between the
finger and thumb so as to compress the
transverse arch of the foot. This is
referred to as Mulders Sign.[citation needed]
There are other causes of pain in the
forefoot. Too often all forefoot pain is
categorized as neuroma. Other conditions
to consider are capsulitis, which is an
inflammation of ligaments that surrounds
two bones, at the level of the joint. In this
case, it would be the ligaments that
attach the phalanx (bone of the toe) to
the metatarsal bone. Inflammation from
this condition will put pressure on an
otherwise healthy nerve and give
neuroma-type symptoms. Additionally, an
intermetatarsal bursitis between the third
and fourth metatarsal bones will also give
neuroma-type symptoms because it too
puts pressure on the nerve. Freiberg's
disease, which is an osteochondritis of the
metatarsal head, causes pain on weight
bearing or compression.[citation needed]

Histopathology
Microscopically, the affected nerve is
markedly distorted, with extensive
concentric perineural fibrosis. The
arterioles are thickened and occlusion by
thrombi are occasionally present.[8][9]

Imaging
Though a neuroma is a soft tissue
abnormality and will not be visualized on
standard radiographs, the first step in the
assessment of forefoot pain is an X-ray in
order to evaluate for the presence of
arthritis and exclude stress
fractures/reactions and focal bone lesions,
which may mimic the symptoms of a
neuroma. Ultrasound (sonography)
accurately demonstrates thickening of the
interdigital nerve within the web space of
greater than 3mm, diagnostic of a
Mortons neuroma. This typically occurs at
the level of the intermetatarsal ligament.
Frequently, intermetatarsal bursitis
coexists with the diagnosis. Other
conditions that may also be visualized
with ultrasound and can be clinically
confused with a neuroma include
synovitis/capsulitis from the adjacent
metatarsophalangeal joint, stress
fractures/reaction, and plantar plate
disruption.[10][11] MRI can similarly
demonstrate the above conditions;
however, in the setting where more than
one abnormality coexists, ultrasound has
the added advantage of determining
which may be the source of the patients
pain by applying direct pressure with the
probe. Further to this, ultrasound can be
used to guide treatment such as cortisone
injections into the webspace, as well as
alcohol ablation of the nerve.

Treatment
Orthotics and corticosteroid injections are
widely used conservative treatments for
Mortons neuroma. In addition to
traditional orthotic arch supports, a small
foam or fabric pad may be positioned
under the space between the two affected
metatarsals, immediately behind the bone
ends. This pad helps to splay the
metatarsal bones and create more space
for the nerve so as to relieve pressure and
irritation. It may however also elicit mild
uncomfortable sensations of its own, such
as the feeling of having an awkward
object under one's foot. Corticosteroid
injections can relieve inflammation in
some patients and help to end the
symptoms. For some patients, however,
the inflammation and pain recur after
some weeks or months, and
corticosteroids can only be used a limited
number of times because they cause
progressive degeneration of ligamentous
and tendinous tissues.
Sclerosing alcohol injections are an
increasingly available treatment
alternative if the above management
approaches fail. Dilute alcohol (4%) is
injected directly into the area of the
neuroma, causing toxicity to the fibrous
nerve tissue. Frequently, treatment must
be performed 24 times, with 13 weeks
between interventions. An 60-80%
success rate has been achieved in clinical
studies, equal to or exceeding the success
rate for surgical neurectomy with fewer
risks and less significant recovery. If done
with more concentrated alcohol under
ultrasound guidance, the success rate is
considerably higher and fewer repeat
procedures are needed.[12]
Radio Frequency Ablation is also used in
the treatment of Morton's Neuroma [13]
The outcomes appear to be equally or
more reliable than alcohol injections
especially if the procedure is done under
ultrasound guidance
2)TARSAL TUNNEL:
Tarsal tunnel syndrome (TTS), also
known as posterior tibial neuralgia, is a
compression neuropathy and painful foot
condition in which the tibial nerve is
compressed as it travels through the
tarsal tunnel.[1] This tunnel is found along
the inner leg behind the medial malleolus
(bump on the inside of the ankle). The
posterior tibial artery, tibial nerve, and
tendons of the tibialis posterior, flexor
digitorum longus, and flexor hallucis
longus muscles travel in a bundle through
the tarsal tunnel. Inside the tunnel, the
nerve splits into three different segments.
One nerve (calcaneal) continues to the
heel, the other two (medial and lateral
plantar nerves) continue on to the bottom
of the foot. The tarsal tunnel is delineated
by bone on the inside and the flexor
retinaculum on the outside.
Patients with TTS typically complain of
numbness in the foot radiating to the big
toe and the first 3 toes, pain, burning,
electrical sensations, and tingling over the
base of the foot and the heel.[1]
Depending on the area of entrapment,
other areas can be affected. If the
entrapment is high, the entire foot can be
affected as varying branches of the tibial
nerve can become involved. Ankle pain is
also present in patients who have high
level entrapments. Inflammation or
swelling can occur within this tunnel for a
number of reasons. The flexor retinaculum
has a limited ability to stretch, so
increased pressure will eventually cause
compression on the nerve within the
tunnel. As pressure increases on the
nerves, the blood flow decreases. [1]
Nerves respond with altered sensations
like tingling and numbness. Fluid collects
in the foot when standing and walking
and this makes the condition worse. As
small muscles lose their nerve supply
they can create a cramping feeling.

Symptoms
Some of the symptoms are:

Pain and tingling in and around

ankles and sometimes the toes

Swelling of the feet

Painful burning, tingling, or numb

sensations in the lower legs. Pain
worsens and spreads after standing
for long periods; pain is worse with
activity and is relieved by rest.

Electric shock sensations

Pain radiating up into the leg,[1] and

down into the arch, heel, and toes

Hot and cold sensations in the feet

A feeling as though the feet do not

have enough padding

Pain while operating automobiles

Pain along the Posterior Tibial nerve

path

Burning sensation on the bottom of

foot that radiates upward reaching
the knee

"Pins and needles"-type feeling and

increased sensation on the feet

A positive Tinel's sign[1]

Tinel's sign is a tingling electric shock

sensation that occurs when you tap over
an affected nerve. The sensation usually
travels into the foot but can also travel up
the inner leg as well.

Cause
It is difficult to determine the exact cause
of Tarsal Tunnel Syndrome. It is important
to attempt to determine the source of the
problem. Treatment and the potential
outcome of the treatment may depend on
the cause. Anything that creates pressure
in the Tarsal Tunnel can cause TTS. This
would include benign tumors or cysts,
bone spurs, inflammation of the tendon
sheath, nerve ganglions, or swelling from
a broken or sprained ankle. Varicose veins
(that may or may not be visible) can also
cause compression of the nerve. TTS is
more common in athletes and other
active people. These people put more
stress on the tarsal tunnel area. Flat feet
may cause an increase in pressure in the
tunnel region and this can cause nerve
compression. Those with lower back
problems may have symptoms. Back
problems with the L4, L5 and S1 regions
are suspect and might suggest a "Double
Crush" issue: one "crush" (nerve pinch or
entrapment) in the lower back, and the
second in the tunnel area. In some cases,
TTS can simply be idiopathic.[1]

Treatment
Treatments typically include rest,
manipulation, strengthening of tibialis
anterior, tibialis posterior, peroneus and
short toe flexors, casting with a walker
boot, corticosteroid and anesthetic
injections, hot wax baths, wrapping,
compression hose, and orthotics.
Medications may include various anti-
inflammatories such as Anaprox, or other
medications such as Ultracet, Neurontin
and Lyrica. Lidocaine patches are also a
treatment that helps some patients.
Conservative treatment (nonsurgical)
There are multiple ways that tarsal tunnel
can be treated and the pain can be
reduced. The initial treatment, whether it
be conservative or surgical, depends on
the severity of the tarsal tunnel and how
much pain the patient is in. There was a
study done that treated patients
diagnosed with tarsal tunnel syndrome
with a conservative approach. Meaning
that the program these patients were
participated in consisted of physiotherapy
exercises and orthopedic shoe inserts in
addition to that program. There were
fourteen patients that had supplementary
tibial nerve mobilization exercises. They
were instructed to sit on the edge of a
table in a slumped position, have their
ankle taken into dorsiflexion and ankle
eversion then the knee was extended and
flexed to obtain the optimal tibial nerve
mobilization. Patients in both groups
showed positive progress from both
programs.[17] The medial calcaneal, medial
plantar and lateral plantar nerve areas all
had a reduction in pain after successful
nonoperative or conservative treatment.
[18]
There is also the option of localized
steroid or cortisone injection that may
reduce the inflammation in the area,
therefore relieving pain. Or just a simple
reduction in the patients weight to
reduce the pressure in the area.[19]

Tarsal Tunnel release

If non-invasive treatment measures fail,
tarsal tunnel release surgery may be
recommended to decompress the area.
The incision is made behind the ankle
bone and then down towards but not as
far as the bottom of foot. The Posterior
Tibial nerve is identified above the ankle.
It is separated from the accompanying
artery and vein and then followed into the
tunnel. The nerves are released. Cysts or
other space-occupying problems may be
corrected at this time. If there is scarring
within the nerve or branches, this is
relieved by internal neurolysis. Neurolysis
is when the outer layer of nerve wrapping
is opened and the scar tissue is removed
from within nerve
3)METATARSALGIA: Metatarsalgia,
literally metatarsal pain and colloquially
known as a stone bruise, is a general
term used to refer to any painful foot
condition affecting the metatarsal region
of the foot. This is a common problem
that can affect the joints and bones of the
metatarsals.
Metatarsalgia is most often localized to
the first metatarsal head the ball of the
foot just behind the big toe. There are two
small sesamoid bones under the first
metatarsal head. The next most frequent
site of metatarsal head pain is under the
second metatarsal. This can be due to
either too short a first metatarsal bone or
to "hypermobility of the first ray"
metatarsal bone and medial cuneiform
bone behind it both of which result in
excess pressure being transmitted into
the second metatarsal head.
3)SKIN DISORDERS
1)CORN AND CALLUSES:

Corns and calluses are hard, thickened

areas of skin that form as a consequence
of rubbing, friction or pressure on the
skin.

Corns and calluses form on the feet and

can make walking painful.

Although corns and calluses are often

talked about together, they are separate
conditions.
Corns generally occur on the tops and
sides of the toes. A hard corn is a small
patch of thickened, dead skin with a small
plug of skin in the centre. A soft corn has
a much thinner surface, appears whitish
and rubbery, and usually occurs between
the toes. Seed corns are clusters of tiny
corns that can be very tender if they are
on a weight-bearing part of the foot. Seed
corns tend to occur on the bottom of the
feet, and some doctors believe this
condition is caused by blocked sweat
ducts.
Calluses are hard and rough-feeling
areas of skin that can develop on hands,
feet or anywhere there is repeated friction
- even on a violinist's chin. Like corns,
calluses have several variants. The
common callus usually occurs when there
has been a lot of rubbing against the
hands or feet. A plantar callus is found on
the bottom of the foot.

What causes corns and calluses?

Some corns and calluses on the feet develop

from an improper walking motion, but most are
caused by ill-fitting shoes. High-heeled shoes
are the worst offenders. They put pressure on the
toes and make women four times as likely as
men to have foot problems. Other risk factors
for developing a corn or callus include foot
deformities and wearing shoes or sandals
without socks, which leads to friction on the
feet.

Rubbing or pressure can cause either soft corns

or plantar calluses. If you or your child develops
a callus that has no clear source of pressure,
have it looked at by a doctor or a podiatrist,
since it could be a wart or be caused by a foreign
body - such as a splinter - trapped under the
skin. Feet spend most of their time in a closed,
moist environment, which is ideal for breeding
fungal and bacterial infections. Staph (bacterial)
infections can start when bacteria enter corns
through breaks in the skin and cause the infected
skin to discharge fluid or pus.

What are the symptoms of corns and

calluses?

A callus is a patch of compact, dead skin

anywhere on the body that is subject to
friction. There are different common
names given to various types of calluses.

A hard corn is a compact patch of hard

skin with a dense core, located on top of
a toe or the outside of the little toe.

A soft corn is a reddened, tender area of

skin, has a thin, smooth centre and is
found between toes.

A seed corn is a plug-like circle of dead

skin, often painful, on the heel or ball of
the foot.

A plantar callus is a callus on the

bottom - or plantar - surface of the foot.

TREATMENT:
Most corns and calluses gradually
disappear when the friction or pressure
stops, although your doctor may shave
the top of a callus to reduce the
thickness. Properly positioned moleskin
pads can help relieve pressure on a corn.
There are also special corn and callus
removal liquids and plasters, usually
containing salicylic acid, but these are not
suitable for everyone.

Oral antibiotics generally clear up infected

corns, but pus may have to be drained
through a small incision.

Moisturising creams may help soften the

skin and remove cracked calluses. Apply
the moisturising cream to the callus, and
cover the area for 30-60 minutes with a
plastic bag or a sock - but only if
instructed to do so by your doctor or
podiatrist.

Then gently rub off as much of the callus

as you can with a coarse towel or soft
brush. Using a pumice stone first to rub
off the dead skin from a callus after a bath
or shower and then applying moisturising
cream can also be effective.

There are also stronger creams containing

urea that might be more effective, but do
not use these unless recommended by
your doctor or podiatrist. Do not use
hydrocortisone creams, which only help
with rashes and itching and are not
needed for calluses. Moisturising your skin
incorrectly can aggravate a fungal
condition and should be avoided -
especially moisturising between the toes.

You may consider surgery to remove a

plantar callus, but there are no
guarantees that the callus will not come
back. A conservative approach is best
initially. Keep your feet dry and friction-
free. Wear properly fitted shoes and
cotton socks, rather than wool or
synthetic fibres that might irritate the
skin.

If a podiatrist (a foot specialist) or

orthopaedic specialist (a bone and joint
specialist) thinks your corn or callus is
caused by abnormal foot structure, your
walking motion or hip rotation,
orthopaedic shoe inserts or surgery to
correct foot deformities may help correct
the problem.
2)ATHELETES FOOT:
Athlete's foot, known medically as tinea
pedis, is a common skin infection of the
feet caused by fungus.[2] Signs and
symptoms often include itching, scaling,
and redness.[3] In severe cases the skin
may blister.[4] Athlete's foot fungus may
infect any part of the foot, but most often
grows between the toes.[3] The next most
common area is the bottom of the foot.[4]
The same fungus may also affect the nails
or the hands.[5] It is a member of the
group of diseases known as tinea.[6]
Tinea pedis is caused by a number of
different fungi.[3] These include species of
Trichophyton, Epidermophyton, and
Microsporum.[5] The condition is typically
acquired by coming into contact with
infected skin, or fungus in the
environment.[3] Common places where the
fungi can survive are around swimming
pools and in locker rooms.[7] They may
also be spread from other animals.[8]
Usually diagnosis is made based on signs
and symptoms; however, it can be
confirmed either by culture or seeing
hyphae using a microscope.[5]
Some methods of prevention include
avoiding walking barefoot in public
showers, keeping the toenails short,
wearing big enough shoes, and changing
socks daily.[5][8] When infected, the feet
should be kept dry and clean and wearing
sandals may help.[3] Treatment can be
either with antifungal medication applied
to the skin such as clotrimazole or for
persistent infections antifungal
medication that are taken by mouth such
as terbinafine.[2][5] The use of the cream is
typically recommended for four weeks. [5]
Athletes foot was first medically described
in 1908.[9] Globally, athlete's foot affects
about 15% of the population.[2] Males are
more often affected than females.[5] It
occurs most frequently in older children or
younger adults.[5] Historically it is believed
to have been a rare condition, that
became more frequent in the 1900s due
to the great use of shoes, health clubs,
war, and travel.[10]

Signs and symptoms

Athlete's foot
Athlete's foot is divided into four
categories or presentations: chronic
interdigital athlete's foot, plantar (chronic
scaly) athlete's foot (aka "moccasin foot"),
acute ulcerative tinea pedis,[11] and
vesiculobullous athlete's foot.[2][12][13]
"Interdigital" means between the toes.
"Plantar" here refers to the sole of the
foot. The ulcerative condition includes
macerated lesions with scaly borders.[11]
Maceration is the softening and breaking
down of skin due to extensive exposure to
moisture. A vesiculobullous disease is a
type of mucocutaneous disease
characterized by vesicles and bullae
(blisters). Both vesicles and bullae are
fluid-filled lesions, and they are
distinguished by size (vesicles being less
than 510 mm and bulla being larger than
510 mm, depending upon what definition
is used).
Athlete's foot occurs most often between
the toes (interdigital), with the space
between the fourth and fifth digits most
commonly afflicted.[14][15][16] Cases of
interdigital athlete's foot caused by
Trichophyton rubrum may be
symptomless, it may itch, or the skin
between the toes may appear red or
ulcerative (scaly, flaky, with soft and
white if skin has been kept wet),[6][17] with
or without itching. An acute ulcerative
variant of interdigital athlete's foot caused
by T. mentagrophytes is characterized by
pain, maceration of the skin, erosions and
fissuring of the skin, crusting, and an odor
due to secondary bacterial infection.[13]
Plantar athlete's foot (moccasin foot) is
also caused by T. rubrum which typically
causes asymptomatic, slightly
erythematous plaques (areas of redness
of the skin) to form on the plantar surface
(sole) of the foot that are often covered
by fine, powdery hyperkeratotic scales.[2]
[13]

The vesiculobullous type of athlete's foot

is less common and is usually caused by
T. mentagrophytes and is characterized
by a sudden outbreak of itchy blisters and
vesicles on an erythematous base,[6]
usually appearing on the sole of the foot.
This subtype of athlete's foot is often
complicated by secondary bacterial
infection by Streptococcus pyogenes or
Staphylococcus aureus.[13]
Complications
As the disease progresses, the skin may
crack, leading to bacterial skin infection[13]
and inflammation of the lymphatic
vessels.[11] If allowed to grow for too long,
athlete's foot fungus may spread to infect
the toenails,[18] feeding on the keratin in
them, a condition called onychomycosis.
[19]

Because athlete's foot may itch, it may

also elicit the scratch reflex, causing the
host to scratch the infected area before
he or she realizes it. Scratching can
further damage the skin and worsen the
condition by allowing the fungus to more
easily spread and thrive. The itching
sensation associated with athlete's foot
can be so severe that it may cause hosts
to scratch vigorously enough to inflict
excoriations (open wounds), which are
susceptible to bacterial infection. Further
scratching may remove scabs, inhibiting
the healing process.
Scratching infected areas may also spread
the fungus to the fingers and under the
fingernails. If not washed away soon
enough, it can infect the fingers and
fingernails, growing in the skin and in the
nails (not just underneath). After
scratching, it can be spread to wherever
the person touches, including other parts
of the body and to one's environment.
Scratching also causes infected skin
scales to fall off into one's environment,
leading to further possible spread.
When athlete's foot fungus or infested
skin particles spread to one's environment
(such as to clothes, shoes, bathroom, etc.)
whether through scratching, falling, or
rubbing off, not only can they infect other
people, they can also reinfect (or further
infect) the host they came from. For
example, infected feet infest one's socks
and shoes which further expose the feet
to the fungus and its spores when worn
again.
The ease with which the fungus spreads
to other areas of the body (on one's
fingers) poses another complication.
When the fungus is spread to other parts
of the body, it can easily be spread back
to the feet after the feet have been
treated. And because the condition is
called something else in each place it
takes hold (e.g., tinea corporis (ringworm)
or tinea cruris (jock itch)), persons
infected may not be aware it is the same
disease.
Some individuals may experience an
allergic response to the fungus called an
id reaction in which blisters or vesicles
can appear in areas such as the hands,
chest, and arms.[20] Treatment of the
underlying infection typically results in
the disappearance of the id reaction.[20]

Causes
Athlete's foot is a form of
dermatophytosis (fungal infection of the
skin), caused by dermatophytes, fungi
(most of which are mold) which inhabit
dead layers of skin and digests keratin.[2]
Dermatophytes are anthropophilic,
meaning these parasitic fungi prefer
human hosts. Athlete's foot is most
commonly caused by the molds known as
Trichophyton rubrum and T.
mentagrophytes,[21] but may also be
caused by Epidermophyton floccosum.[22]
[23]
Most cases of athlete's foot in the
general population are caused by T.
rubrum; however, the majority of athlete's
foot cases in athletes are caused by T.
mentagrophytes.[13]
Transmission
According to the National Health Service,
"Athletes foot is very contagious and can
be spread through direct and indirect
contact."[24] The disease may spread to
others directly when they touch the
infection. People can contract the disease
indirectly by coming into contact with
contaminated items (clothes, towels, etc.)
or surfaces (such as bathroom, shower, or
locker room floors). The fungi that causes
athlete's foot can easily spread to one's
environment. Fungi rub off of fingers and
bare feet, but also travel on the dead skin
cells that continually fall off the body.
Athlete's foot fungi and infested skin
particles and flakes may spread to socks,
shoes, clothes, to other people, pets (via
petting), bed sheets, bathtubs, showers,
sinks, counters, towels, rugs, floors, and
carpets.
When the fungus has spread to pets, it
can subsequently spread to the hands and
fingers of people who pet them. If a pet
frequently gnaws upon itself, it might not
be fleas it is reacting to, it may be the
insatiable itch of tinea.
One way to contract athlete's foot is to
get a fungal infection somewhere else on
the body first. The fungi causing athlete's
foot may spread from other areas of the
body to the feet, usually by touching or
scratching the affected area, thereby
getting the fungus on the fingers, and
then touching or scratching the feet.
While the fungus remains the same, the
name of the condition changes based on
where on the body the infection is
located. For example, the infection is
known as tinea corporis ("ringworm")
when the torso or limbs are affected or
tinea cruris (jock itch or dhobi itch) when
the groin is affected. Clothes (or shoes),
body heat, and sweat can keep the skin
warm and moist, just the environment the
fungus needs to thrive.
Risk factors
Besides being exposed to any of the
modes of transmission presented above,
there are additional risk factors that
increase one's chance of contracting
athlete's foot. Persons who have had
athlete's foot before are more likely to
become infected than those who have
not. Adults are more likely to catch
athlete's foot than children. Men have a
higher chance of getting athlete's foot
than women.[25] People with diabetes or
weakened immune systems[25] are more
susceptible to the disease. HIV/AIDS
hampers the immune system and
increases the risk of acquiring athlete's
foot. Hyperhidrosis (abnormally increased
sweating) increases the risk of infection
and makes treatment more difficult.[26]

Diagnosis

Microscopic view of cultured athlete's foot

fungus
When visiting a doctor, the basic
diagnosis procedure applies. This includes
checking the patient's medical history and
medical record for risk factors,[11] a
medical interview during which the doctor
asks questions (such as about itching and
scratching), and a physical examination.
[11]
Athlete's foot can usually be diagnosed
by visual inspection of the skin and by
identifying less obvious symptoms such
as itching of the affected area.
If the diagnosis is uncertain, direct
microscopy of a potassium hydroxide
preparation of a skin scraping (known as a
KOH test) can confirm the diagnosis of
athlete's foot and help rule out other
possible causes, such as candidiasis,
pitted keratolysis, erythrasma, contact
dermatitis, eczema, or psoriasis.[13][23][27]
Dermatophytes known to cause athlete's
foot will demonstrate multiple septate
branching hyphae on microscopy.[13]
A Wood's lamp (black light), although
useful in diagnosing fungal infections of
the scalp (tinea capitis), is not usually
helpful in diagnosing athlete's foot, since
the common dermatophytes that cause
this disease do not fluoresce under
ultraviolet light.[14]

Prevention
There are several preventive foot hygiene
measures that can prevent athlete's foot
and reduce recurrence. Some of these
include keeping the feet dry, clipping
toenails short; using a separate nail
clipper for infected toenails; using socks
made from well-ventilated cotton or
synthetic moisture wicking materials (to
soak moisture away from the skin to help
keep it dry); avoiding tight-fitting
footwear, changing socks frequently; and
wearing sandals while walking through
communal areas such as gym showers
and locker rooms.[7][13][28]
According to the Centers for Disease
Control and Prevention, "Nails should be
clipped short and kept clean. Nails can
house and spread the infection."[29]
Recurrence of athlete's foot can be
prevented with the use of antifungal
powder on the feet.[13]
The fungi (molds) that cause athlete's foot
require warmth and moisture to survive
and grow. There is an increased risk of
infection with exposure to warm, moist
environments (e.g., occlusive footwear
shoes or boots that enclose the feet) and
in shared humid environments such as
communal showers, shared pools, and
treatment tubs.[17] Chlorine bleach is a
disinfectant and common household
cleaner that kills mold. Cleaning surfaces
with a chlorine bleach solution prevents
the disease from spreading from
subsequent contact. Cleaning bathtubs,
showers, bathroom floors, sinks, and
counters with bleach helps prevent the
spread of the disease, including
reinfection.
Keeping socks and shoes clean (using
bleach in the wash) is one way to prevent
fungi from taking hold and spreading.
Avoiding the sharing of boots and shoes is
another way to prevent transmission.
Athlete's foot can be transmitted by
sharing footwear with an infected person.
Hand-me-downs and purchasing used
shoes are other forms of shoe-sharing.
Not sharing also applies to towels,
because, though less common, fungi can
be passed along on towels, especially
damp ones.

Treatment
Athlete's foot resolves without medication
(resolves by itself) in 3040% of cases. [30]
Topical antifungal medication consistently
produce much higher rates of cure.[31]
Conventional treatment typically involves
thoroughly washing the feet daily or twice
daily, followed by the application of a
topical medication. Because the outer
skin layers are damaged and susceptible
to reinfection, topical treatment generally
continues until all layers of the skin are
replaced, about 26 weeks after
symptoms disappear. Keeping feet dry
and practicing good hygiene (as described
in the above section on prevention) is
crucial for killing the fungus and
preventing reinfection.
Treating the feet is not always enough.
Once socks or shoes are infested with
fungi, wearing them again can reinfect (or
further infect) the feet. Socks can be
effectively cleaned in the wash by adding
bleach. Washing with bleach may help
with shoes, but the only way to be
absolutely certain that one cannot
contract the disease again from a
particular pair of shoes is to dispose of
those shoes.
To be effective, treatment includes all
infected areas (such as toenails, hands,
torso, etc.). Otherwise, the infection may
continue to spread, including back to
treated areas. For example, leaving fungal
infection of the nail untreated may allow it
to spread back to the rest of the foot, to
become athlete's foot once again.
Allylamines such as terbinafine are
considered more efficacious than azoles
for the treatment of athlete's foot.[13][32]
Severe or prolonged fungal skin infections
may require treatment with oral
antifungal medication.
Topical treatments
There are many topical antifungal drugs
useful in the treatment of athlete's foot
including: miconazole nitrate,
clotrimazole, tolnaftate (a synthetic
thiocarbamate), terbinafine hydrochloride,
[17]
butenafine hydrochloride and
undecylenic acid. The fungal infection
may be treated with topical antifungal
agents, which can take the form of a
spray, powder, cream, or gel. Topical
application of an antifungal cream such as
terbinafine once daily for one week or
butenafine once daily for two weeks is
effective in most cases of athlete's foot
and is more effective than application of
miconazole or clotrimazole.[23] Plantar-
type athlete's foot is more resistant to
topical treatments due to the presence of
thickened hyperkeratotic skin on the sole
of the foot.[13] Keratolytic and humectant
medications such as urea, salicyclic acid
(Whitfield's ointment), and lactic acid are
useful adjunct medications and improve
penetration of antifungal agents into the
thickened skin.[13] Topical glucocorticoids
are sometimes prescribed to alleviate
inflammation and itching associated with
the infection.[13]
A solution of 1% potassium permanganate
dissolved in hot water is an alternative to
antifungal drugs.[33] Potassium
permanganate is a salt and a strong
oxidizing agent.
Oral treatments
For severe or refractory cases of athlete's
foot oral terbinafine is more effective than
griseofulvin.[2] Fluconazole or itraconazole
may also be taken orally for severe
athlete's foot infections.[2] The most
commonly reported adverse effect from
these medications is gastrointestinal
upset
TOE DISORDERS:
1)HAMMER TOES:
A hammer toe or contracted toe is a
deformity of the proximal interphalangeal
joint of the second, third, or fourth toe
causing it to be permanently bent,
resembling a hammer. Mallet toe is a
similar condition affecting the distal
interphalangeal joint.[1][2]
Claw toe is another similar condition,
with dorsiflexion of the proximal phalanx
on the lesser metatarsophalangeal joint,
combined with flexion of both the
proximal and distal interphalangeal joints.
Claw toe can affect the second, third,
fourth, or fifth toes.

Causes
Hammer toe most frequently results from
wearing poorly fitting shoes that can force
the toe into a bent position, such as
excessively high heels or shoes that are
too short or narrow for the foot. Having
the toes bent for long periods of time can
cause the muscles in them to shorten,
resulting in the hammer toe deformity.
This is often found in conjunction with
bunions or other foot problems (e.g., a
bunion can force the big toe to turn
inward and push the other toes). It can
also be caused by muscle, nerve, or joint
damage resulting from conditions such as
osteoarthritis, rheumatoid arthritis, stroke,
CharcotMarieTooth disease, complex
regional pain syndrome or diabetes.[3]
Hammer toe can also be found in
Friedreich's ataxia (GAA trinucleotide
repeat).
Treatment
In many cases, conservative treatment
consisting of physical therapy and new
shoes with soft, spacious toe boxes is
enough to resolve the condition, while in
more severe or longstanding cases
podiatric surgery may be necessary to
correct the deformity. The patient's doctor
may also prescribe some toe exercises
that can be done at home to stretch and
strengthen the muscles. For example, the
individual can gently stretch the toes
manually, or use the toes to pick things
up off the floor. While watching television
or reading, one can put a towel flat under
the feet and use the toes to crumple it.
The doctor can also prescribe a brace that
pushes down on the toes to force them to
stretch out their muscle

2) Onychomycosis
From Wikipedia, the free encyclopedia
Onychomycosis
Synony dermatophytic onychomycosis[1] tinea
ms unguium[1]

Onychomycosis, also known as tinea

unguium, is a fungal infection of the nail.
[2]
This condition may affect toenails or
fingernails, but toenail infections are
particularly common.
Treatment may be based on the signs.[3]
Treatment may be with the medication
terbinafine.[3]
It occurs in about 10 percent of the adult
population.[4] It is the most common
disease of the nails and constitutes about
half of all nail abnormalities.[5] The term is
from Ancient Greek (nux) nail +
(mks) fungus + - (-sis)
functional disease.

Signs and symptoms

A case of fungal infection of the big toe

The most common symptom of a fungal
nail infection is the nail becoming
thickened and discoloured: white, black,
yellow or green. As the infection
progresses the nail can become brittle,
with pieces breaking off or coming away
from the toe or finger completely. If left
untreated, the skin can become inflamed
and painful underneath and around the
nail. There may also be white or yellow
patches on the nailbed or scaly skin next
to the nail,[6] and a foul smell.[7] There is
usually no pain or other bodily symptoms,
unless the disease is severe.[8] People with
onychomycosis may experience
significant psychosocial problems due to
the appearance of the nail, particularly
when fingers which are always visible
rather than toenails are affected.[9]
Dermatophytids are fungus-free skin
lesions that sometimes form as a result of
a fungus infection in another part of the
body. This could take the form of a rash or
itch in an area of the body that is not
infected with the fungus. Dermatophytids
can be thought of as an allergic reaction
to the fungus.

Causes
The causative pathogens of
onychomycosis are all in the fungus
kingdom and include dermatophytes,
Candida (yeasts), and nondermatophytic
molds.[10] Dermatophytes are the fungi
most commonly responsible for
onychomycosis in the temperate western
countries; while Candida and
nondermatophytic molds are more
frequently involved in the tropics and
subtropics with a hot and humid climate.
[11]

Dermatophytes
Trichophyton rubrum is the most common
dermatophyte involved in onychomycosis.
Other dermatophytes that may be
involved are T. interdigitale,
Epidermophyton floccosum, T. violaceum,
Microsporum gypseum, T. tonsurans, T.
soudanense A common outdated name
that may still be reported by medical
laboratories is Trichophyton
mentagrophytes for T. interdigitale. The
name T. mentagrophytes is now restricted
to the agent of favus skin infection of the
mouse; though this fungus may be
transmitted from mice and their danders
to humans, it generally infects skin and
not nails.
Other
Other causative pathogens include
Candida and nondermatophytic molds, in
particular members of the mold genus
Scytalidium (name recently changed to
Neoscytalidium), Scopulariopsis, and
Aspergillus. Candida species mainly cause
fingernail onychomycosis in people whose
hands are often submerged in water.
Scytalidium mainly affects people in the
tropics, though it persists if they later
move to areas of temperate climate.
Other molds more commonly affect
people older than 60 years, and their
presence in the nail reflects a slight
weakening in the nail's ability to defend
itself against fungal invasion.
Risk factors
Aging is the most common risk factor for
onychomycosis due to diminished blood
circulation, longer exposure to fungi, and
nails which grow more slowly and thicken,
increasing susceptibility to infection. Nail
fungus tends to affect men more often
than women, and is associated with a
family history of this infection.
Other risk factors include perspiring
heavily, being in a humid or moist
environment, psoriasis, wearing socks and
shoes that hinder ventilation and do not
absorb perspiration, going barefoot in
damp public places such as swimming
pools, gyms and shower rooms, having
athlete's foot (tinea pedis), minor skin or
nail injury, damaged nail, or other
infection, and having diabetes, circulation
problems, which may also lead to lower
peripheral temperatures on hands and
feet, or a weakened immune system. [12]

Diagnosis
To avoid misdiagnosis as nail psoriasis,
lichen planus, contact dermatitis, nail bed
tumors such as melanoma, trauma, or
yellow nail syndrome, laboratory
confirmation may be necessary.[10] The
three main approaches are potassium
hydroxide smear, culture and histology.[10]
This involves microscopic examination
and culture of nail scrapings or clippings.
Recent results indicate the most sensitive
diagnostic approaches are direct smear
combined with histological examination,
[13]
and nail plate biopsy using periodic
acid-Schiff stain.[14] To reliably identify
nondermatophyte molds, several samples
may be necessary.[15]
Classification
There are four classic types of
onychomycosis:[16]

Distal subungual onychomycosis is

the most common form of tinea
unguium[10] and is usually caused
by Trichophyton rubrum, which
invades the nail bed and the
underside of the nail plate.

White superficial onychomycosis

(WSO) is caused by fungal invasion
of the superficial layers of the nail
plate to form "white islands" on the
plate. It accounts for around 10
percent of onychomycosis cases. In
some cases, WSO is a misdiagnosis
of "keratin granulations" which are
not a fungus, but a reaction to nail
polish that can cause the nails to
have a chalky white appearance. A
laboratory test should be
performed to confirm.[17]

Proximal subungual onychomycosis

is fungal penetration of the newly
formed nail plate through the
proximal nail fold. It is the least
common form of tinea unguium in
healthy people, but is found more
commonly when the patient is
immunocompromised.[10]

Candidal onychomycosis is Candida

species invasion of the fingernails,
 usually occurring in persons who
frequently immerse their hands in
water. This normally requires the
prior damage of the nail by
infection or trauma.

Differential diagnosis
Other conditions that may appear similar
to onychomycosis include: psoriasis,
normal aging, yellow nail syndrome, and
chronic paronychia.[18]

Treatment

A person's foot with a fungal nail infection

ten weeks into a course of terbinafine oral
medication. Note the band of healthy
(pink) nail growth behind the remaining
infected nails.
In approximately half of suspected nail
fungus cases there is actually no fungal
infection, but only nail deformity. [19]
Because of this, a confirmation of fungal
infection should precede treatment.[19]
Avoiding use of oral antifungal therapy in
persons without a confirmed infection is a
particular concern because of the side
effects of that treatment, and because
persons without an infection should not
have this therapy.[19] Screening cases
diagnosed by signs and symptoms is not
cost-effective and routine testing is not
necessary for oral treatment with
terbinafine but should be encouraged
prior to topical treatment with
efinaconazole.[20]
Medications
Most treatments are topical or oral
antifungal medications.[4]
Topical agents include ciclopirox nail
paint, amorolfine or efinaconazole.[21][22][23]
Some topical treatments need to be
applied daily for prolonged periods (at
least 1 year).[22] Topical amorolfine is
applied weekly.[24] Topical ciclopirox results
in a cure in 6% to 9% of cases; amorolfine
might be more effective.[4][22] Ciclopirox
when used with terbinafine appears to be
better than either agent alone.[4]
Oral medications include terbinafine (76%
effective), itraconazole (60% effective)
and fluconazole (48% effective).[4] They
share characteristics that enhance their
effectiveness: prompt penetration of the
nail and nail bed,[25] persistence in the nail
for months after discontinuation of
therapy.[26] Ketoconazole by mouth is not
recommended due to side effects. [27] Oral
terbinafine is better tolerated than
itraconazole.[28] For superficial white
onychomycosis, systemic rather than
topical antifungal therapy is advised.

FOOT DROP:
Foot drop is a gait abnormality in which the
dropping of the forefoot happens due to
weakness, irritation or damage to the common
fibular nerve including the sciatic nerve, or
paralysis of the muscles in the anterior portion
of the lower leg. It is usually a symptom of a
greater problem, not a disease in itself. It is
characterized by inability or impaired ability to
raise the toes or raise the foot from the ankle
(dorsiflexion). Foot drop may be temporary or
permanent, depending on the extent of muscle
weakness or paralysis and it can occur in one or
both feet. In walking, the raised leg is slightly
bent at the knee to prevent the foot from
dragging along the ground. Foot drop can be
caused by nerve damage alone or by muscle or
spinal cord trauma, abnormal anatomy, toxins or
disease. Toxins include organophosphorus
compounds which have been used as pesticides
and as a chemical agent in warfare. The poison
can lead to further damage to the body such as a
neurodegenerative disorder called
organophosphorus induced delayed
polyneuropathy. This disorder causes loss of
function of the motor and sensory
neuropathways. In this case, foot drop could be
the result of paralysis due to neurological
dysfunction. Diseases that can cause foot drop
include direct hit to posterolateral neck of fibula,
stroke, amyotrophic lateral sclerosis (ALS or
Lou Gehrig's Disease), muscular dystrophy,
Charcot Marie Tooth disease, multiple sclerosis,
cerebral palsy, hereditary spastic paraplegia,
GuillainBarr syndrome and Friedreich's
ataxia. It may also occur as a result of hip
replacement surgery or knee ligament
reconstruction surgery.

Signs and symptoms

Foot drop is characterized by steppage gait.[1]
While walking, people suffering the condition
drag their toes along the ground or bend their
knees to lift their foot higher than usual to avoid
the dragging.[2] This serves to raise the foot high
enough to prevent the toe from dragging and
prevents the slapping.[3][4] To accommodate the
toe drop, the patient may use a characteristic
tiptoe walk on the opposite leg, raising the thigh
excessively, as if walking upstairs, while letting
the toe drop. Other gaits such as a wide outward
leg swing (to avoid lifting the thigh excessively
or to turn corners in the opposite direction of the
affected limb) may also indicate foot drop.[5]
Patients with painful disorders of sensation
(dysesthesia) of the soles of the feet may have a
similar gait but do not have foot drop. Because
of the extreme pain evoked by even the slightest
pressure on the feet, the patient walks as if
walking barefoot on hot sand.

Diagnosis
Initial diagnosis often is made during routine
physical examination. Such diagnosis can be
confirmed by a medical professional such as a
neurologist, osteopath, orthotist, chiropractor,
physiotherapist, physiatrist, podiatrist,
orthopedic surgeon or neurosurgeon. A person
with foot drop will have difficulty walking on
his or her heels because he will be unable to lift
the front of the foot (balls and toes) off the
ground. Therefore, a simple test of asking the
patient to dorsiflex may determine diagnosis of
the problem. This is measured on a 0-5 scale that
observes mobility. The lowest point, 0, will
determine complete paralysis and the highest
point, 5, will determine complete mobility.
There are other tests that may help determine the
underlying etiology for this diagnosis. Such tests
may include MRI, MRN, or EMG to assess the
surrounding areas of damaged nerves and the
damaged nerves themselves, respectively. The
nerve that communicates to the muscles that lift
the foot is the peroneal nerve. This nerve
innervates the anterior muscles of the leg that
are used during dorsi flexion of the ankle. The
muscles that are used in plantar flexion are
innervated by the tibial nerve and often develop
tightness in the presence of foot drop. The
muscles that keep the ankle from supination (as
from an ankle sprain) are also innervated by the
peroneal nerve, and it is not uncommon to find
weakness in this area as well. Paraesthesia in the
lower leg, particularly on the top of the foot and
ankle, also can accompany foot drop, although it
is not in all instances.
A common yoga kneeling exercise, the
Varjrasana has, under the name "yoga foot
drop," been linked to foot drop.[6][7]

Pathophysiology
The causes of foot drop, as for all causes of
neurological lesions, should be approached
using a localization-focused approach before
etiologies are considered. Most of the time, foot
drop is the result of neurological disorder; only
rarely is the muscle diseased or nonfunctional.
The source for the neurological impairment can
be central (spinal cord or brain) or peripheral
(nerves located connecting from the spinal cord
to an end-site muscle or sensory receptor). Foot
drop is rarely the result of a pathology involving
the muscles or bones that make up the lower leg.
The anterior tibialis is the muscle that picks up
the foot. Although the anterior tibialis plays a
major role in dorsiflexion, it is assisted by the
fibularis tertius, extensor digitorum longus and
the extensor halluces longus. If the drop foot is
caused by neurological disorder all of these
muscles could be affected because they are all
innervated by the deep fibular (peroneal) nerve,
which branches from the sciatic nerve. The
sciatic nerve exits the lumbar plexus with its
root arising from the fifth lumbar nerve space.
Occasionally, spasticity in the muscles opposite
the anterior tibialis, the gastrocnemius and
soleus, exists in the presence of foot drop,
making the pathology much more complex than
foot drop. Isolated foot drop is usually a flaccid
condition. There are gradations of weakness that
can be seen with foot drop, as follows:
0=complete paralysis, 1=flicker of contraction,
2=contraction with gravity eliminated alone,
3=contraction against gravity alone,
4=contraction against gravity and some
resistance, and 5=contraction against powerful
resistance (normal power). Foot drop is different
from foot slap, which is the audible slapping of
the foot to the floor with each step that occurs
when the foot first hits the floor on each step,
although they often are concurrent.
Treated systematically, possible lesion sites
causing foot drop include (going from peripheral
to central):

1. Neuromuscular disease;

2. Peroneal nerve (common, i.e.,

frequent) chemical, mechanical,
disease;

3. Sciatic nervedirect trauma,

iatrogenic;

4. Lumbosacral plexus;

5. L5 nerve root (common, especially

in association with pain in back
radiating down leg);

6. Cauda equina syndrome, which is

cause by impingement of the nerve
roots within the spinal canal distal
to the end of the spinal cord;

7. Spinal cord (rarely causes isolated

foot drop) poliomyelitis, tumor;

8. Brain (uncommon, but often

overlooked) stroke, TIA, tumor;

9. Genetic (as in Charcot-Marie-Tooth

Disease and hereditary neuropathy
with liability to pressure palsies);

10.Nonorganic causes.

If the L5 nerve root is involved, the most

common cause is a herniated disc. Other causes
of foot drop are diabetes (due to generalized
peripheral neuropathy), trauma, motor neuron
disease (MND), adverse reaction to a drug or
alcohol, and multiple sclerosis.
Gait cycle
Drop foot and foot drop are interchangeable
terms that describe an abnormal neuromuscular
disorder that affects the patient's ability to raise
their foot at the ankle. Drop foot is further
characterized by an inability to point the toes
toward the body (dorsiflexion) or move the foot
at the ankle inward or outward. Therefore, the
normal gait cycle is affected by the drop foot
syndrome.
The normal gait cycle is as follows:

Swing phase (SW): The period of

time when the foot is not in contact
with the ground. In those cases
where the foot never leaves the
ground (foot drag), it can be
defined as the phase when all
portions of the foot are in forward
motion.

Initial contact (IC): The point in the

gait cycle when the foot initially
makes contact with the ground; this
represents the beginning of the
stance phase. It is suggested that
heel strike not be a term used in
clinical gait analysis as in many
circumstances initial contact is not
made with the heel. Suggestion:
Should use foot strike.

Terminal contact (TC): The point in

the gait cycle when the foot leaves
the ground: this represents the end
of the stance phase or beginning of
the swing phase. Also referred to as
foot off. Toe-off should not be used
in situations where the toe is not
the last part of the foot to leave the
ground.
The drop foot gait cycle requires more
exaggerated phases.

Drop foot SW: If the foot in motion

happens to be the affected foot,
there will be greater flexion at the
knee to accommodate the inability
to dorsiflex. This increase in knee
extension will cause a stair
climbing movement.

Drop foot IC: Initial contact of the

foot that is in motion will not have
normal heel-toe foot strike. Instead
the foot may either slap the ground
or the entire foot may be planted
on the ground all at once.

Drop foot TC: Terminal contact that

is observed in patients that have
drop foot is quite different. Since
patients tend to have weakness in
the affected foot, they may not
have the ability to support their
body weight. Often, a walker or
cane will be used to assist in this
aspect.

Drop Foot is the inability to dorsiflex, evert, or

invert the foot. So when looking at the Gait
cycle, the part of the gait cycle that involves
most dorsiflexion action would be Heel Contact
of the foot at 10% of Gait Cycle, and the entire
swing phase, or 60-100% of the Gait Cycle. This
is also known as Gait Abnormalities.

Treatment.
The underlying disorder must be treated. For
example, if a spinal disc herniation in the low
back is impinging on the nerve that goes to the
leg and causing symptoms of foot drop, then the
herniated disc should be treated. If the foot drop
is the result of a peripheral nerve injury, a
window for recovery of 18 months to 2 years is
often advised. If it is apparent that no recovery
of nerve function takes place, surgical
intervention to repair or graft the nerve can be
considered, although results from this type of
intervention are mixed.
Non-surgical treatments for spinal stenosis
include a suitable exercise program developed
by a physical therapist, activity modification
(avoiding activities that cause advanced
symptoms of spinal stenosis), epidural
injections, and anti-inflammatory medications
like ibuprofen or aspirin. If necessary, a
decompression surgery that is minimally
destructive of normal structures may be used to
treat spinal stenosis.
Non-surgical treatments for this condition are
very similar to the non-surgical methods
described above for spinal stenosis. Spinal
fusion surgery may be required to treat this
condition, with many patients improving their
function and experiencing less pain.
Nearly half of all vertebral fractures occur
without any significant back pain. If pain
medication, progressive activity, or a brace or
support does not help with the fracture, two
minimally invasive procedures - vertebroplasty
or kyphoplasty - may be options.

Dynamic advanced orthosis for drop foot

Ankles can be stabilized by lightweight
orthoses, available in molded plastics as well as
softer materials that use elastic properties to
prevent foot drop. Additionally, shoes can be
fitted with traditional spring-loaded braces to
prevent foot drop while walking. Regular
exercise is usually prescribed.
Functional electrical stimulation (FES) is a
technique that uses electrical currents to activate
nerves innervating extremities affected by
paralysis resulting from spinal cord injury (SCI),
head injury, stroke and other neurological
disorders. FES is primarily used to restore
function in people with disabilities. It is
sometimes referred to as Neuromuscular
electrical stimulation (NMES) The latest
treatments include stimulation of the peroneal
nerve, which lifts the foot when you step. Many
stroke and multiple sclerosis patients with foot
drop have had success with it. Often, individuals
with foot drop prefer to use a compensatory
technique like steppage gait or hip hiking as
opposed to a brace or splint.
Treatment for some can be as easy as an
underside "L" shaped foot-up ankle support
(ankle-foot orthoses). Another method uses a
cuff placed around the patient's ankle, and a
topside spring and hook installed under the
shoelaces. The hook connects to the ankle cuff
and lifts the shoe up when the patient walks.
TRENCH FOOT:
Trench foot is a medical condition caused by
prolonged exposure of the feet to damp,
unsanitary, and cold conditions. It is one of
many immersion foot syndromes. The use of the
word trench in the name of this condition is a
reference to trench warfare, mainly associated
with World War I, which started in 1914.

Signs and symptoms

Affected feet may become numb, affected by
erythema (turning red) or cyanosis (turning
blue) as a result of poor blood supply, and may
begin emanating a decaying odour if the early
stages of necrosis (tissue death) set in. As the
condition worsens, feet may also begin to swell.
Advanced trench foot often involves blisters and
open sores, which lead to fungal infections; this
is sometimes called tropical ulcer (jungle rot). If
left untreated, trench foot usually results in
gangrene, which may require amputation. If
trench foot is treated properly, complete
recovery is normal, though it is marked by
severe short-term pain when feeling returns.[1]

Causes
Unlike frostbite, trench foot does not require
freezing temperatures; it can occur in
temperatures up to 16 Celsius (about 60
Fahrenheit) and within as few as 13 hours.[2]
Exposure to these environmental conditions
causes deterioration and destruction of the
capillaries and leads to morbidity of the
surrounding flesh.[3] Excessive sweating
(hyperhidrosis) has long been regarded as a
contributory cause; unsanitary, cold, and wet
conditions can also cause trench foot.[4]

Prevention
Trench foot can be prevented by keeping the feet
clean, warm, and dry. It was also discovered in
World War I that a key preventive measure was
regular foot inspections; soldiers would be
paired and each made responsible for the feet of
the other, and they would generally apply whale
oil to prevent trench foot. If left to their own
devices, soldiers might neglect to take off their
own boots and socks to dry their feet each day,
but if it were the responsibility of another, this
became less likely.[5] Later on in the war,
instances of trench foot began to decrease,
probably as a result of the introduction of the
aforementioned measures; of wooden
duckboards to cover the muddy, wet, cold
ground of the trenches; and of the increased
practice of troop rotation, which kept soldiers
from prolonged time at the front.[citation needed]

Treatment
The mainstay of treatment, like the
treatment of gangrene, is surgical
debridement, and often includes
amputation.
INGROWN NAILS:
Onychocryptosis (from Greek onyx "nail"
+ kryptos "hidden"), also known as an
ingrown toenail, or unguis incarnates,[1] is a
common form of nail disease. It is an often
painful condition in which the nail grows so that
it cuts into one or both sides of the paronychium
or nail bed.
The common opinion is that the nail enters
inside the paronychium, but an ingrown toenail
can simply be overgrown toe skin.[2] The
condition starts from a microbial inflammation
of the paronychium, then a granuloma, which
results in a nail buried inside of the granuloma.
[citation needed]
While ingrown nails can occur in the
nails of both the hands and the feet, they occur
most commonly with the toenails.
A true ingrown toenail, or onychocryptosis, is
caused by the actual penetration of flesh by a
sliver of nail.[3]

Signs and symptoms

Symptoms of an ingrown nail include pain along
the margins of the nail (caused by
hypergranulation that occurs around the
aforementioned margins), worsening of pain
when wearing tight footwear, and sensitivity to
pressure of any kind, even the weight of
bedsheets. Bumping of an affected toe can
produce sharp and even excruciating pain as the
tissue is punctured further by the nail. By the
very nature of the condition, ingrown nails
become easily infected unless special care is
taken early to treat the condition by keeping the
area clean. Signs of infection include redness
and swelling of the area around the nail,
drainage of pus, and watery discharge tinged
with blood. The main symptom is swelling at the
base of the nail on the side the nail is ingrowing
(may be both sides).
Ingrown nail should not be confused with a
similar nail disorder: convex nail, named
onychocyrtosis (from Greek onyx "nail" +
kyrtos "convex")[citation needed].[need quotation to
verify]
Nor with other painful nail conditions such
as involuted nails, or the presence of small
corns, callus or debris down the nail sulci
(grooves on either side of the nail plate) or under
the nail plate itself.[4]

Causes
The main cause of onychocryptosis is footwear,
particularly ill-fitting, that includes shoes with
inadequate toe-box room and tight stockings that
apply pressure to the top or side of the foot.[5][6]
Other causes may include the damp atmosphere
of enclosed shoes, which soften the nail-plate
and cause swelling on the epidermal keratin,
which eventually increases the convex arch
permanently, genetics, trauma, and disease.
Improper cutting of the nail may cause the nail
to cut into the side-fold skin from growth and
impact, whether or not the nail is "ingrown"
(true onychocryptosis). The nail bends inwards
or upwards depending on the angle of its cut. If
the cutting tool, such as scissors, is in an attitude
where the lower blade is closer to the toe than
the upper blade, that will cause the toenail to
grow upwards from its base, and vice versa. The
process is visible along the nail as it grows,
appearing as a warp advancing to the end of the
nail. The upper corners turn more easily than the
center of the nail tip. As people cut their nails by
holding the tool always at the same angle, they
induce these conditions by accident; as the nail
turns closer to the skin, it becomes harder to fit
the lower blade in the right attitude under the
nail. When cutting a nail, it is not just the correct
angle that is important, but also how short it is
cut. A shorter cut will bend the nail more, unless
the cut is even on both top and bottom of the
nail.
Causes may include:
 Shoes causing a bunching of the
toes in the developmental stages of
the foot (frequently in people under
21), which can cause the nail to
curl and dig into the skin. This is
particularly the case in ill-fitting
shoes that are too narrow or too
short, but any toed shoes may
cause an ingrown nail.

Poor nail-care, including cutting the

nail too short, rounded off at the tip
or peeled off at the edges instead
of being cut straight across, or
breaking a toenail.

Trauma to the nail plate or toe,

which can occur by stubbing the
toenail, dropping things on the toe
or going through the end of the
shoes (as during sports or other
vigorous activity), can cause the
flesh to become injured and the nail
to grow irregularly and press into
the flesh

Predisposition, such as abnormally

shaped nail beds, nail deformities
caused by diseases, or a genetic
susceptibility increases the chance
of an ingrown nail, but the ingrowth
cannot occur without pressure from
a shoe.

A bacterial infection, treatable with

antibiotics. See "treatments".

One study compared patients with ingrown

toenails to healthy controls and found no
difference in the shape of toenails between
patients and the control group, they suggested
that treatment should not be based on the
correction of a non-existent nail deformity.[7]
Ingrown toenails are caused by weight-bearing
(activities such as walking, running, etc.) in
patients that have too much soft skin tissue on
the sides of their nail. Weight bearing causes this
excessive amount of skin to bulge up along the
sides of the nail. The pressure on the skin around
the nail results in the tissue being damaged,
resulting in swelling, redness and infection. In
the past (and currently) the most common
treatments are mainly directed at the nail
(paradigm paralysis). Treatments often include
part or full removal of the nail. Since the nail is
normal and the problem of too much skin
around the nail was not treated, the results are;
return of the problem, a deformity in the nail, or
the mutilation of the nail.

Prevention
The most common place for ingrown nails is in
the big toe, but ingrowth can occur on any nail.
Ingrown nails can be avoided by cutting nails
straight across; not along a curve, not too short,
and no shorter than the flesh around it. Footwear
that is too small or too narrow, or with too
shallow of a 'toe box', will exacerbate any
underlying problem with a toenail. Sharp square
corners may be uncomfortable and cause
snagging on socks. Proper cutting leaves the
leading edge of the nail free of the flesh,
precluding it from growing into the toe. Filing of
the corner is reasonable. Some nails require
cutting of the corners far back to remove edges
that dig into the flesh, this is often done as a
partial wedge resection at a podiatrist's office.
Ingrown toe nails can be caused by injury,
commonly blunt trauma where the flesh is
pressed against the nail causing a small cut that
swells. Also, injury to the nail can cause it to
grow abnormally, making it wider or thicker
than normal or even bulged or crooked.
Management
The treatment of an ingrown toenail partly
depends on how severe it is.[8]
Conservative treatment
In mild to moderate cases conservative treatment
with warm water and salt soaks, antibacterial
ointment, and the use of dental floss, or a gutter
splint to provide a track along which the nail
may grow is possible. If conservative treatment
of a minor ingrown toenail does not succeed or
if the ingrown toenail is severe, surgical
treatment may be required.[8] A "gutter splint"
may be improvised by slicing a cotton tipped
wooden applicator diagonally to form a bevel
and using this to insert a wisp of cotton from the
applicator head under the nail to lift it from the
underlying skin after a foot soak.[9]
Surgery
Main article: Surgical treatment of
ingrown toenails

A toe post wedge resection with an image

of the nail removed
Surgical treatment for ingrown nails are done by
foot and ankle specialists. This is typically an in-
office procedure requiring local anesthesia and
special surgical instruments. The surgical
approach is a partial nail avulsion of the medial
and lateral nail plate known as a "partial wedge
resection".[8] If the ingrown toenail recurs
despite this treatment, destruction of the sides of
the nail with chemicals or excision is done; this
is known as a matrixcestomy.[8] Antibiotics may
be used post procedure but are not
recommended as they may delay healing.[8]
Nail bracing
A less widely used treatment for ingrown
toenails is nail bracing. Nail braces work by
gently lifting the sides of the toenail and
eventually retraining the nail to grow to a flatter
shape over time. The total time needed for the
nail to be reshaped is one full nail growth or
about 18 months.[10] There are two main types of
nail braces: adhesive and hooked. Adhesive nail
braces are generally made of a thin strip of
composite material that is glued to the top of the
nail. The strip naturally tries to return to a flat
state and lifts the edges of the nails in the
process. Hooked nail braces consist of a hook
(usually made of dental wire) placed under
either side of the nail with some type of
tensioning system pulling the hooks together.
Due to the curved shape of the nail, the
tensioning device rests on the higher middle of
the nail by applying upward pressure to the sides
of the nail. In studies of diabetics, who need to
avoid surgery when possible, nail bracing was
found to be effective at providing immediate
relief as well as long term relief
Neuropathic arthropathy (or neuropathic
osteoarthropathy), also known as Charcot
joint (often "Charcot foot"), refers to
progressive degeneration of a weight bearing
joint, a process marked by bony destruction,
bone resorption, and eventual deformity. Onset
is usually insidious.
If this pathological process continues
unchecked, it can result in joint deformity,
ulceration and/or superinfection, loss of
function, and in the worst-case scenario,
amputation or death. Early identification of joint
changes is the best way to limit morbidity.

Pathogenesis
Any condition resulting in decreased peripheral
sensation, proprioception, and fine motor
control:

Diabetes mellitus neuropathy (the

most common in the U.S. today,
resulting in destruction of foot and
ankle joints), with Charcot joints in
1/600-700 diabetics. Related to
long-term poor glucose control.

Alcoholic neuropathy

Cerebral palsy

Leprosy

Syphilis (tabes dorsalis), caused by

the organism Treponema pallidum

Spinal cord injury

Myelomeningocele

Syringomyelia

Intra-articular steroid injections

Congenital insensitivity to pain

Peroneal muscular atrophy

Underlying mechanisms

Two primary theories have been

advanced:

o Neurotrauma: Loss of
peripheral sensation and
proprioception leads to
repetitive microtrauma to
the joint in question; this
damage goes unnoticed by
the neuropathic patient, and
 the resultant inflammatory
resorption of traumatized
bone renders that region
weak and susceptible to
further trauma. In addition,
poor fine motor control
generates unnatural
pressure on certain joints,
leading to additional
microtrauma.

o Neurovascular: Neuropathic
patients have dysregulated
autonomic nervous system
reflexes, and de-sensitized
joints receive significantly
greater blood flow. The
resulting hyperemia leads to
increased osteoclastic
resorption of bone, and this,
in concert with mechanical
stress, leads to bony
destruction.

In reality, both of these mechanisms probably

play a role in the development of a Charcot
joint.
Joint involvement
Diabetes is the foremost cause in America today
for neuropathic joint disease,[1] and the foot is
the most affected region. In those with foot
deformity, approximately 60% are in the
tarsometatarsal joints (medial joints affected
more than lateral), 30% Metatarsophalangeal
joints and 10% have ankle disease. Over half of
diabetic patients with neuropathic joints can
recall some kind of precipitating trauma, usually
minor.
Patients with neurosyphilis tend to have knee
involvement, and patients with syringomyelia of
the spinal cord may demonstrate shoulder
deformity.
Hip joint destruction is also seen in neuropathic
patients.

Symptoms and signs

Oblique view X-ray in a 45-year-old male

diabetic revealed a divergent, Lisfranc
dislocation of the first metatarsal with
associated lesser metatarsal fractures.

The same 45-year-old man with diabetes

mellitus presented with a diffusely
swollen, warm and non-tender left foot
due to Charcot arthropathy. There are no
changes to the skin itself.
The clinical presentation varies depending on
the stage of the disease from mild swelling to
severe swelling and moderate deformity.
Inflammation, erythema, pain and increased skin
temperature (37 degrees Celsius) around the
joint may be noticeable on examination. X-rays
may reveal bone resorption and degenerative
changes in the joint. These findings in the
presence of intact skin and loss of protective
sensation are pathognomonic of acute Charcot
arthropathy.
Roughly 75% of patients experience pain, but it
is less than what would be expected based on the
severity of the clinical and radiographic
findings.

Clinical findings
Clinical findings include erythema, edema and
increased temperature in the affected joint. In
neuropathic foot joints, plantar ulcers may be
present. Note that it is often difficult to
differentiate osteomyelitis from a Charcot joint,
as they may have similar tagged WBC scan and
MRI features (joint destruction, dislocation,
edema). Definitive diagnosis may require bone
or synovial biopsy.
Radiologic findings
First, it is important to recognize that two types
of abnormality may be detected. One is termed
atrophic, in which there is osteolysis of the distal
metatarsals in the forefoot. The more common
form of destruction is hypertrophic joint disease,
characterized by acute peri-articular fracture and
joint dislocation. According to Yochum and
Rowe, the "6 D's" of hypertrophy are:

1. Distended joint

2. Density increase

3. Debris production

4. Dislocation

5. Disorganization

6. Destruction

The natural history of the joint destruction

process has a classification scheme of its own,
offered by Eichenholtz decades ago:
Stage 0: Clinically, there is joint edema, but
radiographs are negative. Note that a bone scan
may be positive before a radiograph is, making
it a sensitive but not very specific modality.
Stage 1: Osseous fragmentation with joint
dislocation seen on radiograph ("acute
Charcot").
Stage 2: Decreased local edema, with
coalescence of fragments and absorption of fine
bone debris
Stage 3: No local edema, with consolidation and
remodeling (albeit deformed) of fracture
fragments. The foot is now stable.
Destroyed Tarsometatarsal joints in the medial
left foot, with fracture and dislocation of
fragments; these are classic findings. Also note
loss of the foot arch and acquired flat foot (pes
planus) deformity.
Atrophic features:

1. "Licked candy stick" appearance,

commonly seen at the distal aspect
of the metatarsals

2. Diabetic osteolysis

3. Bone resorption

Treatment
Once the process is recognized, it should be
treated via the VIPs vascular management,
infection management and prevention, and
pressure relief. Aggressively pursuing these
three strategies will progress the healing
trajectory of the wound.[2] Pressure relief (off-
loading) and immobilization with total contact
casting (TCC) are critical to helping ward off
further joint destruction.
TCC involves encasing the patients complete
foot, including toes, and the lower leg in a
specialist cast that redistributes weight and
pressure in the lower leg and foot during
everyday movements. This redistributes pressure
from the foot into the leg, which is more able to
bear weight, to protect the wound, letting it
regenerate tissue and heal.[3] TCC also keeps the
ankle from rotating during walking, which
prevents shearing and twisting forces that can
further damage the wound.[4] TCC aids
maintenance of quality of life by helping
patients to remain mobile.[5]
There are two scenarios in which the use of TCC
is appropriate for managing neuropathic
arthropathy (Charcot foot), according to the
American Orthopaedic Foot and Ankle Society.
[6]
First, during the initial treatment, when the
breakdown is occurring, and the foot is
exhibiting edema and erythema; the patient
should not bear weight on the foot, and TCC can
be used to control and support the foot. Second,
when the foot has become deformed and
ulceration has occurred; TCC can be used to
stabilize and support the foot, and to help move
the wound toward healing.
Walking braces controlled by pneumatics are
also used. Surgical correction of a joint is rarely
successful in the long-term in these patients.
However, off-loading alone does not translate to
optimal outcomes without appropriate
management of vascular disease and/or
infection.[7] Duration and aggressiveness of
offloading (non-weight-bearing vs. weight-
bearing, non-removable vs. removable device)
should be guided by clinical assessment of
healing of neuropathic arthropathy based on
edema, erythema, and skin temperature changes.
[8]
It can take 69 months for the edema and
erythema of the affected joint to recede

SUMMAR
Y:
Today I
have
discussed
about
various
foot
disorders
their
causes
treatment
risk factors
and
ptreventio
n
CONCLUS
ION
The feet
are the
 foundation
of our
bodies,
and they
assist us in
some of
the most
basic
functions
of living.
Each foot
contains
26 bones,
which are
controlled
by
multiple
ligaments,
muscles,
and
tendons.[1]
Through
activities
of living,
the feet
can
change
structurall
y over
time,
causing a
reshaping
of the feet
BIBLIOGRAPHY:
BIBLIOGRAPHY:
1)Basavanthapa,medica surgical
nursing,2nd edition,Jaypee brothers
Pg 890-895
2)Dr Sanjay Pandya,practical guidelines of
assessment of the elderly,3rd edition,pg
90-95