High Risk Quiz Flashcards
What is a neuropathic ulcer?
- occurs in pressure areas in an insensate foot
- common where there are structural/biomechanical abnormalities
- common in those with diabetes
What are the characteristics of a neuropathic ulcer?
- even wound margins
- periwound HK
- superficial or deep (can have sinus formation)
- painless (mainly due to lack of sensation)
- pt usually has palpable pulses
How do you treat a neuropathic ulcer?
- offloading is most important
- need to look at biomechanics and correction of structural deformities
- education on neuropathy/diabetes control
- dressings
What is an ischaemic/arterial ulcer?
- a wound that forms due to lack of blood supply to the area
- in combination with arterial insufficiency
- common on the toes, met head, malleoli, and med/lat borders of the foot
What are the characteristics of an ischaemic ulcer?
- demarcated edges
- presence of necrotic tissue
- pale base
- little to no HK
- painful
- absent pedal pulses
How do you treat an ischaemic ulcer?
- refer to vascular surgeon
- if wound is dry then paint with betadine
- if wound is wet then consider wet gangrene
What is a venous ulcer?
- venous ulcers occur when there is chronic venous insufficiency/valve dysfunction that leads to oedema
- the skin becomes thin and weak, and prone to ulceration
- common in the medial/lateral malleolar regions and posterior calf
What are the characteristics of a venous ulcer?
- irregular margins
- nil periwound HK
- nil/mild pain
- dry/thin skin
- hyper pigmentation (red/brown staining)
- pulses are present but can be hard to palpate due to oedema
How do you treat a venous ulcer?
- reduce the oedema e.g. with compression therapy
- address the underlying medical concern (e.g. venous insufficiency)
- encourage activity and ambulation to work muscle pump and optimise venous/lymph return
- dressings
What is a pressure ulcer?
- external pressure causes local ischaemia, cellular death and tissue damage
- elderly and bed ridden are most affected
- can be hospital acquired
- common on posterior heel or bony prominences e.g. trochanter, sacrum, calcaneus, 1st/5th MPJs, malleoli
What are the characteristics of a pressure ulcer?
- skin may be intact on initial presentation, followed by breakdown
- can be superficial or deep extending to subcutaneous tissue, tendon or bone
How do you treat a pressure ulcer?
- prevention! early ID, mobilising patients, foam overlays and air mattresses, resting AFOs, heel lifts/herbst cradle, sheepskin heel protectors, bed cradles
What types of dressings are available and on what type of wound would you use them? (groups)
- semi-permeable films ( superficial/low exudating wounds)
- hydrogels (dry/low exudating wounds)
- hydrocolloids (uninfected low/moderate exudating wounds)
- manuka honey (low/moderately exudating wounds)
- alginates (moderate/high exudating wounds)
- foams (low/high exudating wounds)
- antimicrobials (low/high exudating wounds)
- hydrofiber (high exudating wounds)
- negative pressure wound therapy (non-bleeding non-infected wounds)
Which part of the anatomy is affected by digital deformities?
IPJ, MPJ, tendons, joint capsules and ligamentous structures.
What are the possible aetiologies of digital deformities?
- ill-fitting footwear
- biomechanics of foot
- congenital e.g. long ray
- trauma
- attrition due to synovitis of plantar plate, capsule &/or collateral ligament
- neuromuscular e.g. CMT, CP, MS
- diabetes
- inflammatory disease e.g. RA or Psoriatic arthopathy
All of these factors can lead to an imbalance between the extensor and flexor muscles of the toes, leading to lesser toe deformities.
How does a long metatarsal cause a lesser toe deformity?
It is more prone to injury such as stubbing as it is longer than other toes. In footwear it may buckle.
In which plane is a digital deformity easiest to correct?
Sagittal plane, followed by frontal plane and transverse plane.
What are the possible digital deformities?
- hammer toe
- claw toe
- mallet toe
- digitus adductus
- digitus abductus
- varus toe
What test do you do to classify whether a hammer toe is rigid or flexible?
‘Push up Test’
Rigid - minimal relocation of the base of the phalanx to the met head
Flexible - complete realignment of the deformity
How do the extrinsic and intrinsic muscles work together to keep a toe in rectus alignment?
Extrinsics - extend MPJ and flex IPJ
Intrinsics - flex MPJ and extend IPJ
What are the categories of digital dysfunction?
flexor substitution
flexor stabilisation
extensor substitution
Describe flexor stabilisation in pes planus.
In late stance phase the flexors attempt to stabilise a pronated foot - they fire longer.
Pull of FDL shifts medially - adductovarus of toes 4/5 common.
Describe flexor substitution in pes cavus.
Occurs in a supinated foot in late stance phase.
The flexors try to substitute for a weak triceps surae and overpower the interrossei.
Usually see straight contracture of lesser toes.
Describe extensor substitution.
Evident during swing phase.
EDL gains mechanical advantage over the intrinsics - EDL is becoming main DF of foot for whatever reason.
All lesser toes become contracted and retracted at the MPJs.
What are the surgical goals of correcting digital deformities?
- re-establish a rectus alignment
- stability to resist reoccurrence
- shorten the toe if required
- alleviate pain!
What procedures could be used to correct a hammertoe?
Soft tissue:
May be used in elderly low activity patients or in flexible digital deformity
- V to Y plasty (lengthening of contracted tissue)
- Stab tenotomy (percutaneous flexor tenotomy)
- Extensor tenotomy (isolated)
- Flexor tenotomy (in combination with an osseous correction)
- capsulotomy (release of a tight capsule)
- Flexor tendon transfer (stabilise a digit and decrease dorsiflexed proximal phalanx)
Osseous:
- arthroplasty (remodelling of joint via excision of bone)
- Arthrodesis (fusion of a joint to provide stability)
What procedure could be done to alleviate problems caused by a cross over toe?
Digital amputation of cross over toe.
What procedure could be done to alleviate problems caused by a bone prominence?
Ostectomy - removal of a prominent bone (exostosis)
What is a percutaneous internal fixation and when is it used?
Refers to an exposed pin utilised to maintain stability.
- 3 weeks for arthroplasty, 6 weeks for arthrodesis
What is the aetiology of IGTNs?
- oral retinoids (causes nail to become brittle, slow growing and the skin becomes fragile)
- trauma
- fungal nail infections
- hereditary - HAV, foot type
- genetic factors
- geriatric
What is the aetiology of onychogryphosis?
- trauma
- pressure (e.g. footwear)
- fungal infection
- diabetes
- PVD
- nutritional
- psoriasis
What is the aetiology of onychauxis?
- diabetes
- psoriasis
- PVD
- hereditary
- acromegaly
- infection
- genetic/chronic disorder
What types of nail surgery can be performed for and IGTN?
- nail excision and avulsion
- chemical matrixectomy
- partial excisional matrixectomy
- total excisional matrixectomy
- subungal ostectomy
What are ‘red flags’ for nail surgery?
- diabetes
- paediatrics
- PVD/arterial insufficiency
- blood thinner use
- current infection
In which patients is a subungal exostosis common?
May cause an IGTN.
- 40+
- often involuted nails
- pain on distal dorsal aspect of nail
- may be associated with trauma
In which patients is a subungal osteochondroma common, and what does it cause?
May cause an IGTN.
- teenagers/young adults
- nail plate may appear normal
- suspect when rapid onset
- may be hx of trauma
How may a periungual verrucae be surgically treated?
- partial or total excisional matrixectomy of the nail and wart
What may cause plantar plate deterioration?
- cross over toe
- overlapping hammertoe
- capsulitis
- bursitis
- pre-dislocation syndrome
- metatarsalgia
How does the plantar plate receive nutrition?
Has poor blood supply - relies on synovial fluid.
Where is the plantar plate located?
- in the capsule of the MPJ
- the met head rests directly on it
- 2-3mm thick
Can the plantar plate degenerate?
Yes - pp degenerates with age. Usually degenerates around distal attachment to the proximal phalanx.
Not all worn out or torn pp’s are symptomatic.
What are the signs that the plantar plate is torn?
- pain on palpation of the plantar toe sulcus
- malalignment of digits
- loss of toe purchase
- lateral or medial deviation (if tear is lateral the toe will deviate medially)
What is the clinical classification of plantar plate tears?
Stage 1:
- mild plantar pain and oedema at MPJ
- tenderness with manipulation of joint
- no anatomical malalignment
Stage 2:
- noticeable deviation of toe
- in stance toe isn’t purchasing but it has purchasing power
- positive vertical stress test
Stage 3:
- moderate oedema around whole MPJ
- subluxation and dislocation (cross over toes)
- phalangeal base is in fixed dislocated position
What may lead to a plantar plate tear?
Structural and biomechanical deformities that increase loading in the forefoot:
- long 2nd met
- HAV deformity
- biomechanical hypermobility
What investigations could you order if you suspect a plantar plate tear?
X-rays or ultrasound.
How could you conservatively treat a plantar plate tear?
- taping
- corticosteroid injections (but if do this then toe must be strapped into downward position too) - this would treat associated synovitis
NB: with conservative treatment, while you may treat the pain the deformity may still progress
When would you surgically treat a plantar plate tear?
- when it is not responsive to conservative treatment after 3 months
- if there is a severe deformity
- ultimate surgical aim: a rectus toe with ground gripping strength
What type of surgery would you use to correct a deformity resulting from a plantar plate tear?
Depends on what the deformity is - if a hammertoe, transverse plane deviation, or dislocation/subluxation.
Direct primary repair: stitch the plantar plate back together.
Amputation in really severe cases.
What are the key risk factors for patients with diabetes?
- peripheral neuropathy (sensory, motor, autonomic)
- peripheral arterial disease
- structural deformity
- previous ulceration
What is the common causal pathway for diabetic ulceration?
Neuropathy + Deformity + Minor Trauma (environmental event), over time leading to ulceration
Trauma can be acute or chronic e.g. a cut or continued pressure for footwear.
Ulceration can be life threatening due to…
Sepsis! May lead to multiple organ shut down, and has a significant risk of death.
What are the additional costs associated with ulceration?
- limited mobility
- social isolation
- family issues
- loss of work time
- psychological impact
- septicaemia/bacteremia
- loss of function
- amputation
- health care costs
Early intervention for ulceration involves…
Assessment, Education and Intervention.
Describe what observations need to be made when assessing a wound.
- aetiology
- location
- size/depth
- clinical appearance (wound bed, edges, surrounding tissue)
- exudate (amount/type/colour)
- pain
- presence of infection
- wound classification system e.g. texas
Name the intrinsic factors that affect wound healing.
- age
- mental state
- skin condition
- nutrition
- medical conditions
- infection
Name the extrinsic factors that affect wound healing.
- medications e.g. DMARDs (Methotrexate), corticosteroids
- smoking
- mobility/activity
- pressure
- hygiene
Name some of the common causes of lower extremity wounds.
- arterial insufficiency
- venous insufficiency
- neuropathy
- pressure
- surgical
- burns
- neoplastic disorders (e.g. melanoma)
What disorders can cause peripheral neuropathy?
- Hereditary disorders (e.g. CMT)
- Systemic/Metabolic disorders (e.g. DM, habitual alcohol use)
- Systemic effects of malignancies (e.g. cancers)
- Infections or inflammatory conditions (e.g. HIV, Guillan-Barre)
- Exposure to toxic compounds (e.g. glue sniffing)
- Neuropathy secondary to drug use
- Miscellaneous e.g. trauma (severing of nerve)
What disorders can cause peripheral vascular disease?
- superficial femoral occlusive disease
- tibial artery disease
- atherosclerosis
- smoking
- renal disease
- small vessel disease (e.g. Reynaud’s disease)
What disorders can result in immunosuppression?
- organ transplants
- chemo
- stem cell transplant
Why is offloading an ulcer important?
- increased plantar pressure during ambulation is one of the major causative factors in the development of foot ulcers
- reduced healing time
- reduced risk of infection
- reduced risk of further complications/cost
- better patient outcome/quality of life
Name some different methods of offloading.
- bed rest
- crutches
- wheelchairs
- sheepskin boots (hospital grade ugg boot)
- post-op shoe
- medical grade/custom footwear
- orthoses
- pneumatic/air cast walker
- non-pneumatic walker
- total contact cast
- Charcot Restraint Orthotic Walker (CROW)
- Pressure Relieving Ankle Foot Orthotic
- Herbst Cradle (falls risk as patient cant walk in this - only for use in bed)
Why is patient compliance important to remember when deciding on a method of offloading?
Patient may be able to remove offloading.
They may not understand why they need it, or be motivated to wear it if it impacts daily living/work commitments.
What is the pathogenesis of a Morton’s Neuroma?
- Smaller IM distance: worsened with small toe box, toe off can compress the nerve against IM ligament.
- Met 4/5 more mobile than 2/3
- Intermetatarsal Bursitis: dorsal to transverse metatarsal ligament - bursa compresses nerve to ligament.
What diagnostic tests could you order for a Morton’s Neuroma?
X-ray (rule out #), ultrasound.
What are the conservative treatment methods for a Morton’s Neuroma?
- no treatment
- modified activity
- change of footwear
- functional orthoses (met dome)
- NSAIDs/pain meds
- cortisone/local anaesthetic injections
What are the surgical treatment options for a Morton’s Neuroma?
- Neurectomy - surgical excision (dorsal approach preferred)
Is HAV inheritable?
Yes - highly inheritable
- large IM angle 1-2
- long 1st met
- round 1st met head
- abnormal muscle tendon insertion (tip post, EHL)
- abnormal foot posture (pes cavus/planus)
What are the significant findings associated with HAV?
- pain associated with medial subcutaneous bony prominence
- aggravated by footwear
- great toe laterally deviated often with axial values rotation
- widening of forefoot or splay foot
- need to rule out rheumatoid arthritis
What are some associated findings with HAV?
- hammertoe
- plantar HK
- central metatarsalgia
- onychocryptosis
- neuritis
- knee pain
- self reported arthritis
After which age is HAV likely to progress more quickly?
At age 55… indicates that if going to operate might have better outcomes before 50
What is Juvenile Hallux Valgus?
- onset is before 10 y.o.
- can be surgically corrected - usually delay until skeletal maturity
What classification system is used for HAV?
Manchester Scale - has been validated.
What do you look for when assessing ROM at the 1st MPJ?
- normal ROM is 90 degrees DF
- crepitus or smooth
- flexible/rigid deformity (can you correct it into rectus)
- WBing and NWBing ROM
What conservative treatments are available for HAV?
- waiting
- toe alignment splints at night
- foot exercises
- orthotic therapy
- physical therapy
- width and depth of footwear
What are the surgical options for HAV?
- most evidence for chevron osteotomy
- may need a combination of soft tissue and bone procedures
- Silver procedure (just removes medial bump)
- McBride procedure (soft tissue)
- Reverdin procedure
- Mitchell osteotomy
- first MPJ arthrodesis (long term poor predictability)
What are possible complications of surgical management of HAV
- joint stiffness
- transfer metatarsalgia
What is hallux rigidus?
A term used to describe symptoms commonly associated with degenerative joint disease of the first MPJ.
- stiffness and pain
- no motion
Hallux limitus is when there is <65 degrees dorsiflexion at the 1st MPJ.
Who is OA of the 1st MPJ most common in?
- middle age men
- active (usually runners)
- often bilateral and familial
What are the proposed aetiologies of 1st MPJ OA?
Many theories - most likely multi-factorial
- include long/short 1st met
- long/wide prox phalanx
- trauma
- arthropathies
- plantar fascia contracture
- RF varus
- FF varus
- age
- females
- accessory navicular
- tarsal coalition
How may trauma be a etiological factor for 1st MPJ OA?
- direct macro trauma causes osteochondral fracture
- direct/indirect micro trauma to joint in combination with other predisposing factors
- iatrogenic
How may a muscle spasm contribute to pain in the 1st MPJ?
Muscle spasms immobilise the joints as a protective mechanism to pain. The cyclic process of immobilisation propagates articular degeneration and fusion.
How could a long 1st met cause OA of the 1st MPJ?
- long 1st met disrupts the met parabola and 1st met cannot adequately plantar flex
What are the clinical signs of 1st MPJ OA?
- pain within and around 1st MPJ
- rubor and swelling
- occasionally paraesthesia due to compression of digital nerve
- palpable and visible dorsal, medial & lateral joint osteophyte
- sometimes IPJ hyperextension
What imaging could you order if you suspected 1st MPJ OA?
X-rays… looking for:
- gradual joint destruction
- osteophyte
- joint space narrowing
- articular surface flattening
- subchondral lesions
- sesamoid hypertrophy/osteopenia
- hallux valgus interphalangeus
What are the Ddx for 1st MPJ OA?
- plantar plate injury
- turf toe
- nerve entrapment
- OM/septic arthritis
- Gout
What would you see in a Grade 0 1st MPJ OA?
- no xray changes
- normal joint space
- normal 1st met head and proximal phalanx contouring
What would you see in a Grade 1 1st MPJ OA?
- may be hallux equinus
- peri-articular subchondral sclerosis
- minimal dorsal osteophytes
- minimal 1st met head flattening
- good joint space preservation
What would you see in a Grade 2 1st MPJ OA?
- moderate dorsal osteophytes
- moderate 1st met head flattening
- minimal joint space narrowing
- lateral 1st MPJ exostosis
- may see sesamoid hypertrophy
- may see subchondral cyst formation
What would you see in a Grade 3 1st MPJ OA?
- severe dorsal osteophytes
- moderate 1st met head flattening
- loss of visible joint space
- sesamoid hypertrophy
- sub chondral cyst formation
- intra-articular bone fragments
What would you see in a Grade 4 1st MPJ OA?
- excessive dorsal osteophytes
- minimal/absent joint space
- sesamoid fusion
- subchondral cyst formation
- other OA changes
What are the conservative treatment options for 1st MPJ OA?
- oral or topical NSAIDs
- orthoses to facilitate 1st MPJ motion
- sesamoid mobilisation/flexor strengthening
- intra-articular cortison
When would you be looking to limit joint motion in someone with 1st MPJ OA?
around grade 3 - looking at surgery, orthosis with a Morton’s extension, rocker sole shoes, carbon fibre plates
What types of surgical management are available for those with 1st MPJ OA, and what may dictate your choice of procedure?
Procedure choice dictated by the amount of viable articular cartilage present (over or under 50%) - will be a joint salvage procedure or a joint destruction procedure.
- valente cheilectomy (useful for grade 1-2 HR)
- youngswick-austin osteotomy (useful for grade 1-2 HR)
- silastic interposition arthroplasty (less active patients)
- capsular interposition arthroplasty (advanced HR)
- implant arthroplasty
- semi implant arthroplasty
- arthrodesis (grade 4 HR)
When is an arthrodesis indicated for 1st MPJ OA?
- indicated for grade 4 (end stage HR)
