5: Lower Leg, Ankle and Foot Flashcards

1
Q

what purpose do the bones of the foot serve

A

provide mechanical support for soft tissues, helping foot to withstand the weight og the body whilst standing and in motion

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2
Q

what groups can the bones of the foot be divided into

A
  1. tarsal bones: seven irregularly shaped bones, situated proximally in foot
  2. metatarsals: fice which connect the phalanges to tarsal bones
  3. phalanges: bones of the toes; each toe has 3 phalanges (proximal, middle and distal) except big toe which only has proximal and distal
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3
Q

what three regions can the foot be divided into

A
  1. hindfoot: talus and calcaneus
  2. midfoot: navicular, cuboid, cuneiforms
  3. forefoot: metatarsals and phalanges
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4
Q

what are the three articulations of the talus

A

this is the most superior of the tarsal bones and transmits the weight og the body to the foot
1. superiorly: ankle joint (between the talus, tibia and fibula)
2. Inferiorly: subtalar joint, between the talus and calcaneus.
3. Anteriorly: talonavicular joint, between the talus and the navicular

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5
Q

what is the main function of the talus

A

to transmit forces from tibia –> calcaneus
- trochlear of the talus articulates w the tibia and fibula
- wider anteriorly than posteriorly and this shape provides additional stability to the dorsiflexed ankle

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6
Q

explain the blood supply to the talus

A
  • although numerous ligaments attached to talus, no muscles originate or insert onto it
  • blood supply = retrograde meaning arteries enter bone at distal end
  • lack of muscle attachments improve vascularity and retrograde blood supply = high risk of avascular necrosis if talus fractures
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7
Q

what are the articulations of the calcaneus

A

largest tarsal bone, is inferior to the talus and constitutes the heel
1. Superiorly: subtalar (talocalcaneal) joint, between the calcaneus and the talus
2. Anteriorly: calcaneocuboid joint, between the calcaneus and the cuboid

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8
Q

structure and function of calcaneus

A
  • protrudes posteriorly and takes full weight of body when heel contacts the ground when walking
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9
Q

what is the posterior aspect of the calcaneus marked by

A

calcaneal tuberosity –> Achilles tendon attaches

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10
Q

what are calcaenus and talus sometimes referred to

A

proximal row of tarsal bones

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11
Q

what does the intermediate row of tarsal bones contain

A

navicular
- articulates w talus posteriorly, all three cuneiform bones anteriorly, and the cuboid bone laterally
- on the plantar surface, there is a tuberosity for the insertion of part of the tibialis posterior tendon

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12
Q

what does the distal row of tarsal bones contain

A

four tarsal bones: cuboid. lateral, intermediate and medial cuneiforms
- cuboid = furthest lateral and articulates proximally with the calcaneus and distally with 4th and 5th metatarsals
- inferior/plantar surface of cuboid marked by groove for the tendon of peroneus longus
- three cuneiforms are wedge-shaped and articulate w navicular proximally and 1st three metatarsals distally
- wedge-shape helps to form the transverse arch of the foot

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13
Q

which muscles insert onto the medial cuneiform

A

tibialis anterior, tibialis posterior and peroneus longus

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14
Q

tarsometatarsal joint

A

between metatarsal base and tarsal bone

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15
Q

intermetatarsal joint

A

between metatarsals and adjacent metatarsals

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16
Q

metatarsophalangeal joint

A

between metatarsal head and proximal phalanx

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17
Q

describe the ankle joint

A

ankle or talucrural joint is a synovial joint between bones of the leg (tib fib) and foot (talus)
- functionally a hinge joint allowing dorsiflexion and plantarflexion of the foot

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18
Q

what are the tibia and fibula bound by distally

A

tibiofibular ligaments at the distal tibiofibular joint
- form a bracket-shaped socket known as a mortise
- trochlea of talus fits snugly into ankle mortise aka malleolar fossa

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19
Q

explain what happens in dorsiflexion and plantarflexion

A
  • dorsiflexion: anterior part of the trochlea is held in the mortise and joint = more stable
  • plantarflexion: posterior part of the trochlea is held in the mortise and joint = less table
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20
Q

what muscles produce plantarflexion

A

muscles in posterior compartment of leg
- gastrocnemius, soleus, plantaris and tibialis posterior

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21
Q

what muscles produce dorsiflexion

A

muscles in the anterior compartment
- tibialis anterior, extensor hallucis longus, extensor digitorum longus and peroneus tertius

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22
Q

what is range of dorsiflexion usually limited by

A

passive resistance in muscles of posterior compartment

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23
Q

what is the ankle joint reinforced by

A

lateral and medial ligaments

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24
Q

what are the three parts of the lateral ligament and their function

A
  • resist inversion of the foot
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25
Q

function of the medial/deltoid ligament

A

stronger and resists excessive eversion of the foot
- fibres fan out from medial malleolus to attach to talus, calcaneus and navicular

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26
Q

what is the subtalar joint

A

articulation between talus and calcaneus
- plane type of synovial joint which is on an oblique axis and is the major joint within the foot at which eversion and inversion movements take place

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27
Q

what muscles produce eversion

A

lateral compartment of leg
- peroneus longus and peroneus brevis
anterior compartment of leg
- peroneus tertius

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28
Q

which muscles produce inversion

A

anterior compartment
- tibialis anterior

deep posterior
- tibialis posterior

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29
Q

what are the main weight bearing bones during standing

A

heel and heads of metatarsals

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30
Q

how are the arches of the foot maintained

A

by the shape of the interlocking bones, the ligaments of the foot, the intrinsic muscles of the foot and the pull of the long tendons of extrinsic muscles(i.e. muscles in the anterior, lateral and posterior compartments of the leg)

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31
Q

arches of the foot

A
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32
Q

describe the transverse arch

A

half-arch which makes a full arch when feet are together

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33
Q

describe the medial longitudinal arch

A

most important clinically
- formed by: calcaneus, talus, navicular, three cuneiforms and the medial three metatarsals
- plantar aponeurosis and the spring ligament (plantar calcaneonavicular ligament; binding the calcaneum to the navicular), together with the tibialis anterior and the peroneus (fibularis) longus tendons play major roles in maintaining the integrity of this arch
- muscles supporting the medial longitudinal arch are the tibialis anterior, tibialis posterior, peroneus (fibularis) longus and flexor hallucis longus

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34
Q

describe the lateral longitudinal arch

A
  • formed by: calcaneus, cuboid and lateral two metatarsals
  • ## Contraction of the peroneus (fibularis) brevis muscle may help in supporting the lateral longitudinal arch
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35
Q

what happens to arches in standing/walking position

A
  • standing: arches sink somewhat under the weight of the body, the individual bones lock together, the ligaments binding them are under maximum tension and the foot becomes an immobile ‘pedestal’
  • walking: tension is released from the arches which unlock and become a mobile lever system with a spring-like action
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36
Q

what are the signs and symptoms of compartment syndrome

A
  • severe pain in the limb which is excessive to degree of injury increasing and not relieved by analgesia
  • clasically exacerbated by passive stretch of muscles
  • if compartment syndrome is suspected, surgical decomplression (fasciotomy) should be performed of all affected compartments
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37
Q

what are the short term consequences of compartment syndrome

A
  • increase in intracompartmental pressure leads to decreased perfusion of muscle
  • ischaemic muscle releases mediators which further increase capillary permeability and exacerbate the rise in intracompartmental pressure
  • in severe cases, rhabdomyolysis (muscle necrosis) and acute kidney injury can result
  • neurovascular signs develop late in the process and are often undeveloped at the time of diagnosis
  • compartment pressure exceeds the systolic arterial pressure, there will be loss of peripheral pulses and increased capillary refill time
  • nerve fibres are susceptible to ischaemia; thin cutaneous nerve fibres are affected more quickly than the motor fibres, so distal paraesthesia precedes loss of motor function
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38
Q

what are the long term consequences of compartment syndrome

A
  • rhabdomyolysis can result in acute kidney injury which may become chronic
  • necrotic muscle may also undergo fibrosis leading to Volkmann’s ischaemic contracture, a permanent painful and disabling contracture of the affected muscle groups
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39
Q

define ankle fracture

A

a fracture of any malleolus with or without disruption to the syndesmosis

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40
Q

what else needs to be considered w ankle fractures and why

A

co-morbidities: diabetes, neuroopathy, peripheral vascular disease, smoking
- these are likely to affect fracture healing
- e.g. diabetics have almost doube the fracture healing time of non-diabetics

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41
Q

open ankle fractures

A
  • where skin barrier is breached and there is a direct communication between fracture and external environment
  • common and require urgent surgery w extensive irrigation and debridement to reduce risk of osteomyelitis
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42
Q

how are the ankle joint and associated ligaments arranged

A

can be visualised as a ring in the coronal plane
- proximal: articular surfaces of the tibia and fibula, united at the inferior tibiofibular joint by syndesmotic ligaments
- medial: medial (deltoid) ligament
- inferior: subtalar joint (between the talus and the calcaneus)
- lateral: lateral ligament complex of the ankle (anterior talofibular, talocalcaneal and posterior talofibular)
- important to bear in mind that when a ring breaks, it normally breaks in 2 places so when dealing w single fracture, there is likely to be associated ligament damage not apparent on x-ray
- e.g. injury which results in forced eversion or external rotation of foot will push against the lateral malleolus –> oblique fracture and will pull in ligaments –> ruptured deltoid ligaments/transverse fracture of medial malleolus

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43
Q

explain what is meant by talar shift

A
  • when there is disruption out of any 2 syndesmosis, medial or lateral ligaments, ankle mortise = unstable and widens so that the talus can shift medially or laterally within the ankle joint
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44
Q

how are ankle fractures treated

A
  • stable ankle fractures: treated non-operatively w aircast boot or fibreglass cast
  • patients can bear weigth safely, low rate of complic e.g. secondary OA
  • unstable ankle fractures: need surgical stabilisation which can be high risk in patients w diabtes or peripheral vascular disease
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45
Q

ankle sprain

A

partial or complete tear of one or more ligaments of the ankle joint
- most heal w time and rest but those that dont heal can cause late ankle instability and sometimes require surgery

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46
Q

which factors can contribute to an increased risk of ankle sprains

A
  • Weak muscles/tendons that cross the ankle joint, especially the peroneal muscles
  • Weak or lax ankle ligaments – this can be hereditary or due to overstretching of ligaments as a result of repetitive ankle sprains
  • Inadequate joint proprioception (i.e. sense of joint position)
  • Slow neuromuscular response to an off-balance position
  • Running on uneven surfaces
  • Shoes with inadequate heel support
  • Wearing high-heeled shoes – due to the weak position of the ankle joint with an elevated heel, and a small base of support
47
Q

how do ankle sprains occur

A
  • excessive strain on ligaments of ankle which can be cuased by excessive external rotation, inversion/eversion of foot due to external force
  • foot passes normal range of motion = excess stress puts strain on ligaments
48
Q

what is the most common mechanism of injury in an ankle sprain

A

inversion injury affecting a plantar-flexed and weightbearing foot
- anterior talofibular ligament is most at risk of sprain

49
Q

what is an avulsion fracture

A

when a tendon or ligament is placed under tension and instead of the tendon or ligament tearing, a fragment of bone is pulled off at the insertion site

50
Q

In a severe sprain of the ankle, why is it not uncommon to find that the patient has an avulsion fracture of their fifth metatarsal tuberosity?

A
  • **peroneus (fibularis) brevis tendon **is attached to a tubercle on the base of the 5th metatarsal
  • In an inversion injury, it is under tension and can pull off a fragment of bone at its insertion site
51
Q

in children, what can be confused for a 5th metatarsal fracture

A
  • In children aged approximately 10-16 years, an unfused 5th metatarsal apophysis can often be seen on foot X-rays
  • Examining the child clinically and looking at the orientation of the lucent line on the X-ray will help you differentiate between a fracture and an unfused apophysis.
52
Q

what are mechanisms of injury of an achilles tendon rupture

A
  • Making a forceful push-off with an extended knee (e.g. during jumping)
  • A fall with the foot outstretched in front and the ankle dorsiflexed, forcibly overstretching the tendon
  • Falling from a height, or abruptly stepping into a hole or off a kerb
  • NB: complete tear more common than partial
53
Q

where is the site of rupture in achilles tendon injury

A
  • often the** ‘vascular watershed’ area**, approximately 6cm proximal to the insertion of the Achilles tendon (calcaneal tendon) onto the calcaneal tuberosity
  • this is an area of decreased vascularity and thickness of the tendon, which together render it more susceptible to tearing
54
Q

signs and symptoms of achilles tendon rupture

A
  • A sudden and severe pain at the back of the ankle or in the calf (like being ‘kicked in the heel’)
  • The sound of a loud pop or snap
  • A palpable (and sometimes visible) gap or depression in the tendon
  • Initial pain and swelling followed by bruising
  • Inability to stand on tip toe or to push-off whilst walking
55
Q

how do you test/diagnose for achilles tendon rupture

A

Thompson’s test
- diagnosis can be made clinically, but MRI and ultrasound can also be used very effectively to demonstrate the gap in the Achilles tendon

56
Q

how is achilles tendon rupture treated

A
  • often when tendon ruptures, two ends are frayed which makes surgical reconstruction hard
  • mostly now treated conservatively with the foot being held in the correct position in an aircast boot
  • high complic rate of surgery because overlying skin is thin and poorly vascularised
57
Q

what does hallux valgus involve

A

distal part of the big toe is deviated laterally
* Varus deviation of the first metatarsal
* Valgus deviation and/or lateral rotation of the hallux
* Prominence of the first metatarsal head, with or without an overlying callus

58
Q

causes of hallux valgus

A
  • poor choice of footwear can exacerbate this is if it is already present by keeping hallux in valgus deviation
  • can also occur secondary to trauma, arthritic/metabolic conditions such as gout, rheumatoid arthritis and psoriatic arthritis and to connective tissue disorders that cause ligamentous laxity e.g. Ehlers-Danlos syndrome
  • association with ligamentous laxity probably also explains why bunions tend to ‘run in families’
  • Once present, the line of pull of the extrinsic tendons (e.g. EHL tendon) exacerbates the problem
59
Q

treatment for hallux valgus

A
  • surgery should not be carried out for cosmetic reasons as it may convert normal foot to painful
  • surgery involves metatarsal osteotomy and realigning fragements
  • similar process may also be needed in proximal phalanx of great toe
60
Q

hallux rigidus

A

OA of the 1st metatarsophalangeal joint, resulting in stiffness of this joint
- joint is normally under tremendous stress during walking as, with each step, a force equivalent to twice the body weight passes through this very small joint (prone to developing OA)
- other secondary causes can include gout and previous septic arthritis
- commonest symptom is pain in the MTPJ on walking and on attempted dorsiflexion of the toe
- Patients tend to compensate for the pain by walking on the outside of their foot (i.e. inverting the foot and walking on the lateral border)
- range of dorsiflexion of the toe becomes severely restricted due to the arthritis, although plantar flexion is usually retained

61
Q

what may develop as a result of hallux rigidus

A

dorsal bunion (osteophyte) on top of the joint and rub on patient’s shoes

62
Q

surgical management of OA

A
  • Arthroplasty = joint replacement
  • Arthrodesis = joint fusion
  • Excision arthroplasty = surgical removal of the joint with interposition of soft tissue (e.g. a rolled-up tendon, between the bone ends)
  • Osteotomy = surgical cutting of a bone to allow realignment (to take the load of the affected part of the joint)
63
Q

treatment plan of OA

A
  • initially, treatment of hallux rigidus involves activity modification, analgesia, orthotics or aids and sometimes intra-articular steroid injections
  • rigid sole orthotic is a very stiff shoe insert that prevents motion at the 1st MTPJ: will help prevent the pain caused by dorsiflexion of the toe whilst walking
  • if conservative management fails to control the symptoms sufficiently, surgery may be considered
  • number 1 choice: arthrodesis (fusion) of the 1st MTPJ where joint is excised so that it is effectively replaced by a ‘fracture’. The ‘fracture’ is then stabilised with screws and normal fracture healing subsequently fuses the joint
  • Arthroplasty (replacement) of the 1st MTPJ may be considered and there are now some specialised prostheses available for this joint
64
Q

different types of toe deformities

A
65
Q

claw toe

A
  • often affect all four of the small toes at the same time
  • toes are hyperextended at MTPJ and flexed at PIP joint
  • sometimes also at DIP joint so toes curl under foot
  • corns can develop over dorsum of toe or under head of metatarsal
66
Q

what can cause claw toe

A
  • result from a muscle imbalance which causes ligaments and tendons to become unnaturally tight usually due to neurological damage
  • may be secondary to conditions e.g. cerebral palsy, stroke, diabetes or alcohol dependence
  • trauma, inflammation and arthritis can also cause claw toe
67
Q

hammer toe and mallet toe

description + causes

A
  • hammer toe: a deformity in which the toe is flexed at the proximal interphalangeal joint (PIPJ)
  • mallet toe: toe flexed at the distal interphalangeal joints (DIPJ)
  • causes: ill-fitting pointed shoes, pressure on 2nd toe from adjacent hallux vagus
    - tight shoe causes toe to stay in flexed position for too long so the muscle contracts and shortens so harder to extend toe; over time, muscle cannot extend toe even when shoes not worn
68
Q

curly toes

A
  • congenital and usually involve the 3-5th digits
  • usually bilateral and more common when there is a family history
  • thought to develop because the tendons of the flexor digitorum longus (FDL) or flexor digitorum brevis (intrinsic muscle of foot) are too tight
  • most children = asymptomatic
  • treatment: usually conservative w passive extension of toes and stretching of flexors tendons
  • surgery rarely needed and only considered >6y/o when painful on activity
69
Q

Achilles tendinopathy

A

degnerative and non-inflammatory process
- often follows many years of overuse (e.g. long distance runners, sprinters), especially those whose training regimens are poor
- can also occur in people who are inactive
- risk factors include obesity and diabetes

70
Q

where can achilles tendinopathy develop

A
  • at point of insertion of achilles tendon –> calcaneum (insertional tendinopathy)
  • at vascular ‘watershed’ area within achilles tendon (non-insertional tendinopathy)
71
Q

signs and symptoms of achilles tendinopathy

A
  • Pain and stiffness along the Achilles tendon in the morning
  • Pain in the tendon or at the back of the heel that worsens with activity
  • Severe pain 24 hours after exercising
  • Thickening of the tendon
  • Swelling that is present all of the time but worsens during activity
  • A palpable bone spur (in insertional tendonitis)
72
Q

treatment of achilles tendinopathy

A
  • physiotherapy, especially eccentric stretching exercises, to try and improve the vascularity of the tendon and promote healing
73
Q

flat foot (pes planovalgus)

A
  • implies that the medial arch of the foot has collpased so that the medial border of the foot almost touches the ground
  • valgus refers to valgus angulation of the hindfoot
74
Q

why do most young children appear flat footed

A
  • arches have not developed yet and also large amount of subcutaneous adipose tissue in sole of foot (medial fat pad)
  • medial longitudinal arch of foot begins to form in children around 5y/o
  • so only if deformity persists into adolescence or recurs then abnormal
  • orthotics are ineffective in promoting normal development of arch so should not be prescribed
75
Q

how and why is it important to differentiate between flexible and rigid flat feet

A
  • majority of pt have flexible flat feet meaning they have no medial arch when standing normally but when on tip-toe, a normal medial arch appears and hindfoot returns from valgus deviation into normal alignment
  • rigid flat feet are always abnormal; usually develop as a result of tarsal coalition (failure of the tarsal bones to separate during embryonic development)
  • when patients w rigid flat feet stand on tiptoe, no arch appears and the hindfoot remains in valgus
  • rigid flatfoot is often symptomatic and therefore requires treatment
76
Q

adult acquired flatfoot

A
  • results from dysfunction of tibialis posteiror tendon which usually supports the medial longitudinal arch of foot whilst walking
  • most commonly occurs in middle aged females who give a history of change in shape of foot and pain behind medial malleolus
  • lack of support of medial arch by tibialis posterior leads to stretching of spring ligament (plantar calcaneonavicular ligament) and plantar aponeurosis
  • stretching of ligaments: talar head being displaced inferomedially, flattening the medial longitudinal arch and producing lateral deviation of the hindfoot
  • symptoms improve in 80% of these patients following the use of orthotics (insoles) to support their medial arch and physiotherapy to improve muscle strength
  • some patients either surgical reconstruction or, if secondary OA has developed, arthrodesis of the joints of their hindfoot
77
Q

what is foot disease

A

a common and serious complication of diabetes and includes infection, ulceration or destruction of tissues of foot
- combination of loss of sensation due to peripheral neuropathy; ischaemia due to peripheral arterial disease and microvascular disease; and immunosuppression due to poor glycaemic control can lead to foot ulcers, severe infections and other serious complications
- there is a loss of protective sensation, so the patients will often continue to weight-bear on very significant soft tissue abnormalities, thereby exacerbating the problem

78
Q

how do patients reduce risk of foot disease

A
  • attend regular ‘diabetic foot clinics’ for screening
  • feet checled for any corns, callouses, cracks and dry skin
  • sensation and perfusion of feet are assessed and their shoes checked to make sure they are suitable protective against trauma (strong soles, not open-toed) and fit well
  • educated on how to look after feet and reduce chance of complications
  • tight glycaemic control is also emphasised as being important in preventing development of neuropathy and vascular disease and maintaining a healthy immune response
79
Q

what can poorly controlled diabetes lead to

A

Charcot arthropathy

80
Q

what does Charcot arthropathy involve

A

progressive destruction of bones, joints and soft tissues
- most commonly involved ankle and foot but can affect other jionts e.g. knee
- combination of neuropathy, abnormal loading of foot, repeated microtrauma (w non healing microfractures)
- metabolic abnormalities –> inflammation causing osteolysis (bone resorption), fractures, dislocation and deformity
- as a result of neuropathy, patient = reduced ability to detect touch, temp and pain so may continue to walk on Charcot foot making injury worse
- neuropathy also leads to muscle spasticity e.g. tight Achilles tendon which exacerbates deformity
- severe cases = rocker bottom foot
- pt are often obese which increases load placed through softened bones and usually have poor glycaemic control –> secondary immunosuppression

81
Q

treatment of Charcot arthropathy

A
  • optimisation of glycaemic control and reduction of load placed on affected joints
  • can be challenging as there is reduced bone stock and bones are soft due to inflamm
  • pt do not often experience pain so not reminded to stop weight bearing
82
Q

antalgic gait

A
  • patient walks in manner that reduces pain
  • walk w a limp which shortens the stance phase of the painful limb so spend more time walking on less painful limb and minimise time spent weight-bearing on the affected limb
  • automatically shortens the swing phase in the unaffected limb so uneven gait
83
Q

how do patients with antalgic gait offload a painful imb

A

walking stick used in hand opposite to painful limb
- pt can lean towards walking stick, shift their centre of gravity away from painful limb and reduce load through it during stance phase

84
Q

trendelenburg gait

A
  • normally in the stance phase, hip abductors (gluteus medius and minimus) contract to prevent the pelvis dropping on the unsupported side
  • when this mechanism fails, patient will demonstrate a positive Trendelenburg sign whilst standing on one leg and a trendelenburg gait whilst walking
85
Q

causes of Trendelenburg gait

A
  • superior gluteal nerve lesions
  • ^^ and consequent muscle paralysis as a complication of hip surgery or injections to buttock
  • muscle pain and inhibition of function
  • trauma e.g. fracture or greater trochanter or dislocation of hip joint
  • biomechanical hip instability e.g. developmental dysplasia of hip
86
Q

describe appearance of Trendelenburg gait

A
  • pelvis drops on the unaffected side so patient tries to compensate for this by swinging their torso over towards affected side
  • resulting gait is sometimes describes as ‘waddling
87
Q

cause of hemiplegic gait

A

due to paralysis of one side of body
- most commonly as a result of stroke but also cerebral palsy or trauma to CNS e.g. head or spinal cord injury
- patients have spasticity on affected side
- most severe in flexor muscle of upper limb and extensor muscles of lower limb as these are the dominant muscle groups

88
Q

explain typical presentation of a patient with hemiplegic gait

A
  • flexed upper limb and extended lower limb
  • patient cannot flex their hip, knee or ankle so to take a step, they lean towards unaffected side of body then circumduct the paralysed leg
  • patient cannot bear much weight on paralysed leg so stance phase on limb = very short
  • gait = short step w unaffected leg followed by circumduction of affected leg
89
Q

diplegic gait

A

spasticity affects both lower limbs most commonly due to cerebral palsy
- pt walks w very narrow-based gait dragging both legs and scraping their toes on the ground
- spasticity in the hip adductors can cause legs to cross midline (scissoring)
- spasticity in the hamstrings means knees are slightly flexed
- spasticity in the gastrocnemius and soleus results in plantar-flexion of ankles
- commonly the forefoot that makes inital contact with the ground

90
Q

high steppage gait

A

seen in patients with weakness of ankle dorsiflexion resulting in ‘drop foot’
- when foot raised, absence of active dorsiflexion means the foot assumes a position of plantarflexion under the effect of gravity
- so much more hip flexion required to lift foot high off ground and stop toes dragging floor
- in initial contact,** normal eccentric contraction** of tibialis anterior muscle is absent so foot slaps down onto ground

91
Q

causes of high steppage gait (3)

A
  1. common peroneal nerve palsy: e.g. trauma to nerve following fracture, compression of nerve against fibular neck
  2. sciatica
  3. neuromuscular disease e.g. Charcot-Marie-Tooth disease
92
Q

what happens if deep peroneal nerce is damaged but superficial peroneal nerve is intact

A

instead of a classical high-steppage gait, the patient may compensate for the lack of dorsiflexion during the swing phase by everting their foot in a sudden motion, called an eversion flick

93
Q

parkinsonian gait

A
  • parkinson’s disease: nerve cells in subtantia nigra degenerate leading to reduction in dopamine which plays a vital part in regulating body movement
  • pt w parkinson’s find it difficult to initate movement
  • to counteract this they flex their neck and trunk forwards to move their centre of gravity in front of their lower limbs
  • take short steps known as shuffling gait and may also exhibit ‘festinant’ gait - tendency to take accelerating steps
  • typically have loss of arm swing whilst walking
94
Q

ataxic gait

A

clumsy, staggering movements with a broad-base (feet wide apart)
- patients often hold arms outwards to help them balance
- whilst standing still, pt body may sway back and forth and side to side (titubation)
- pt will not be able to walk heel-toe or in straight line

95
Q

three causes of ataxia

A
  1. proprioceptive
  2. cerebellar disease
  3. vestibular
96
Q

causes of cerebellar dysfunction

A
  1. inherited
  2. acquired e.g. stroke
  3. acute alcohol intoxication
97
Q

state the arrangement of structures posterior to the medial malleolus of the ankle from anterior to posterior

A
98
Q

four pulses of the lower limb

A

femoral pulse
- can be palpated as it enters the femoral triangle at the mid-inguinal point (between ASIS and pubic symphysis)
popliteal artery
- hardest to palpate as it lies deep in the popliteal fossa
- ask pt to slightly flex leg which relaxes deep fasica in roof of popliteal fossa
dorsalis pedis
- palpate dorsum of foot, immediately lateral to extensor hallucis longus tendon
posterior tibial pulse
- palpated in tarsal tunnel, just below and behind medial malleolus

99
Q

identify muscles of anterior leg

A
  1. tibialis anterior
  2. extensor digitorum longus
  3. peroneus tertius
  4. extensor hallucis longus
100
Q

what are the muscles of the anterior leg

A
  1. tib anterior
  2. extensor hallucis longus
  3. extensor digitorum longus
  4. peroneus tertius
101
Q

innervation of anterior leg

A

deep peroneal

102
Q

general action of anterior leg

A

dorsiflexion and inversion

103
Q

muscles of lateral leg

A

peroneus longus and brevis

104
Q

innervation of lateral leg

A

superficial peroneal

105
Q

general actions of lateral leg

A

eversion

106
Q

muscles of superficial posterior leg

A

plantaris
soleus
gastrocnemius

107
Q

muscles of deep posterior leg

A

tibialis posterior
flexor hallucis longus
flexor digitorum longus
popliteus

108
Q

general actions of posterior leg

A

plantarflexion and inversion

109
Q

innervation of posterior leg

A

tibial nerve (terminal branch of sciatic nerve)

110
Q

how are ankle fractures classified

A

Weber classification
- A: below the syndesmosis
- B: at level
- C: above level

the more proximal the injury, the higher likelihood of ankle instability so type C fractures almost always need surgical fixation

111
Q

what position must the ankle be in when taking x-rays

A

full dorsiflexion
- the talus is narrower posteriorly so it can appear translated within the mortise when the ankle is plantarflexed

112
Q

what type of ankle fractures require ORIF

A
  • Displaced bimalleolar or trimalleolar fractures
  • Weber C fractures
  • Weber B fractures with talar shift
  • Open fractures
113
Q

what are features of an S1 lesion

A
  • sensory loss of posterolateral aspect of leg and lateral foot
  • weakness in plantarflexion
  • reduced ankle reflex
  • positive sciatic nerve stretch test