Lower Limb Flashcards
Mechanical back pain - define
Mechanical back pain is extremely common.
- It is characterised by pain when the spine is loaded, that worsens with exercise and is relieved by rest. - It tends to be intermittent and is often triggered by innocuous activity.
Mechanical back pain - risk factors
obesity,
poor posture,
a sedentary lifestyle with deconditioning of the paraspinal (core) muscles,
poorly-designed seating
incorrect manual handling (bending and lifting) techniques.
Disc Degeneration & Marginal osteophytosis
The nucleus pulposus of the intervertebral discs dehydrates with age.
This leads to a decrease in the height of the discs, bulging of the discs and alteration of the load stresses on the joints.
Osteophytes (bony spurs) called syndesmophytes therefore develop adjacent to the end plates of the discs. This is known as marginal osteophytosis.
Increased stress is also placed on the facet joints, which also develop osteoarthritic changes. The facet joints are innervated by the meningeal branch of the spinal nerve, so arthritis in these joints is perceived as painful.
As the disc height decreases and arthritis develops in the facet joints and vertebral bodies, the intervertebral foramina decrease in size.
This can lead to compression of the spinal nerves and is perceived as radicular or nerve pain.
what are the 4 stages of disc herniation
- Disc degeneration: chemical changes associated with ageing cause discs to dehydrate and bulge
- Prolapse: Protrusion of the nucleus pulposus occurs with slight impingement into the spinal canal. The nucleus pulposus is contained within a rim of annulus fibrosus
- Extrusion: The nucleus pulposus breaks through the annulus fibrosus but is still contained within the disc space
- Sequestration: The nucleus pulposus separates from the main body of the disc and enters the spinal canal
what nerve is affected of a paracentral hernaition of L4/L5
compression of a spinal nerve root within the intervertebral foramen.
Transverinsg nerve root (nerve root that emerges below)
Aka L5 root affected
what is risk of central herniation?
Cauda equina
directly towards spinal cord
what nerve is affected in far lateral herniation
Exiting nerve root affected (aka L4).
Nerve root that emerges at same level as intervertebral disc
Radicular leg pain
Sciatica is the name given to pain caused by irritation or compression of one or more of the nerve roots that contribute to the sciatic nerve (i.e. L4, L5, S1, S2 and S3).
The pain experienced is typically experienced in the back and buttock and radiates to the dermatome supplied by the affected nerve root. Hence it follows a path ‘from the back to the dermatome
If the nerve compression also causes paraesthesia, this will be only experienced in the affected dermatome (rather than the full path from lumbar spine to dermatome)
L4 sciatica pain distribution
anterior thigh, anterior knee, medial leg
L5 sciatica pain distribution
lateral thigh, lateral leg, dorsum of foot
S1 sciatica pain distriction
posterior thigh, posterior leg, heel, sole of foot
Causes of leg radicular?
marginal osteophytosis,
slipped disc etc
Cauda equina - what is it?
Cauda equina syndrome can develop in the context of prolapsed intervertebral disc when there is a ‘canal filling disc’ that compresses the lumbar and sacral nerve roots within the spinal canal.
Cauda equina - causes
Approx. 5% of cases of cauda equina syndrome are due to a central disc prolapse. 30 – 50 years. tumours (primary or secondary) affecting the vertebral column or meninges, spinal infection / abscess, spinal stenosis secondary to arthritis, vertebral fracture, spinal haemorrhage, late-stage ankylosing spondylitis.
Cauda equina symptoms
Bilateral sciatica Perianal numbness (saddle anaesthesia) Painless retention of urine Urinary / faecal incontinence Erectile dysfunction
Cauda equina Treatment
Cauda equina syndrome needs to be treated by surgical decompression within 48 hours of the onset of sphincter symptoms, otherwise the prognosis is poor.
The consequences of missing this diagnosis are serious and life-changing e.g. chronic neuropathic pain, impotence, having to perform intermittent self-catheterisation to pass urine, faecal incontinence or impaction requiring manual evacuation of the rectum, loss of sensation and lower limb weakness requiring a wheelchair. You do not want to miss a case of cauda equina syndrome
Spinal canal stensosis
abnormal narrowing of the spinal canal that compresses either the spinal cord or the nerve roots
Lumbar stenosis is most common, followed by cervical stenosis.
Spinal cord stenesosis - causes
Spinal canal stenosis tends to affect the elderly and is often due to a combination of:
Disc bulging
Facet joint osteoarthritis
Ligamentum flavum hypertrophy
Other causes include:
Compression fractures of the vertebral bodies
Spondylolisthesis
Trauma
Spinal cord steneosis - symptoms
The symptoms depend on the region of the cord or nerve roots that are affected.
Discomfort whilst standing (95% of patients)
Discomfort or pain in the shoulder, arm or hand (for cervical stenosis) or in the lower limb (for lumbar stenosis)
Bilateral symptoms in approximately 70% of patients
Numbness at or below the level of the stenosis
Weakness at or below the level of the stenosis
Neurogenic claudication (see below)
The natural history of lumbar canal stenosis is that 70% of patients’ symptoms stay unchanged, 15% get progressively worse and 15% improve with time.
Neurogenic claudication
Neurogenic claudication (or pseudoclaudication) is a symptom rather than a diagnosis.
Neurogenic means that the problem originates in the nerve and claudication is derived from the Latin for limp (claudigo), as the patient feels a cramping pain or weakness in their legs, and therefore tends to limp.
It results from compression of the spinal nerves as they emerge from the lumbosacral spinal cord (spinal canal stenosis).
This leads to venous engorgement of the nerve roots during exercise, leading to reduced arterial inflow and transient arterial ischaemia.
The ischaemia of the affected nerve(s) results in the pain and/or paraesthesia.
Neurogenic claudication -symptoms
The patient reports pain and/or pins and needles in the legs on prolonged standing and on walking, radiating in a sciatica distribution.
Neurogenic claudication may be present in one or both legs. It is classically relieved by rest (most effective), a change in position and by flexion of the spine.
Movements that involve flexion of the waist are well tolerated such as cycling, pushing a trolley and climbing stairs.
Spondylolisthesis
Spondylolisthesis is anterior displacement of the vertebra above on the vertebra below. It is classified into various types according the underlying cause
Congenital or dysplastic: congenital instability of the facet joints
Isthmic: A defect in the pars interarticularis
Degenerative: results from facet joint arthritis and joint remodelling (age >50 years)
Traumatic: Acute fractures in the neural arch, other than the pars interarticularis
Pathological: Infection or malignancy
Iatrogenic: Caused by surgical intervention e.g. if too much lamina and facet joint is excised during a laminectomy operation Spondylolisthesis may, or may not, be associated with gross instability of the vertebral column.
Spondylolisthesis -symptoms
Some individuals remain asymptomatic, but most complain of some discomfort ranging from occasional lower back pain to incapacitating mechanical pain, sciatica from nerve root compression, and neurogenic claudication (see next page).
You should be able to recognise spondylolisthesis on an X-ray or MRI scan
Describe a lumbar puncture and how is it performed
Lumbar puncture is the withdrawal of fluid from the subarachnoid space of the lumbar cistern.
It is an important diagnostic test for a variety of central nervous system disorders including meningitis, multiple sclerosis etc.
“Lumbar puncture (LP) is performed with the patient lying on the side with the back and hips flexed (knee–chest position) (fig. 2.40). Flexion of the vertebral column facilitates insertion of the needle by spreading apart the vertebral
laminae and spinous processes, stretching the ligamenta flava. The skin covering the lower lumbar vertebrae is anesthetized, and a lumbar puncture needle is inserted in the midline between the spinous processes of the L3 and L4 (or L4 and L5) vertebrae. This can be located by finding the plane transecting the highest points of the iliac crests—the supracristal plane—this usually passes through the L4 spinous process. At these levels, there is no danger of damaging the spinal cord. After passing 4–6 cm in adults (more in obese persons), the needle “pops” through the ligamentum flavum, then punctures the dura and arachnoid, and enters the lumbar cistern. When the stylet is removed, CSF escapes and can be collected.”
OA - what is it
Clinical syndrome comprising joint pain accompanined by functional limitation and reduced QOL
Affeted joints: hips, knees, cervical spine, lumbar spine, small joints of hands
Chronic disease without sysemic invovlement
○ No invovlement of eyes, skin, etc
○ Non inflammatory
Risk factros leads to excessive/uneven loading of joint = damage to hyaline cartialge covering articular surface
Hyaline cartialge becomes swollen due to increased proteogylcan synthesis by chondrocytes
Increased numbers of chondrocytes differentiating from chondroprogenitor cells (adult chondrocytes do not proliferate)
This is an attempty to repair the cartialge damage and can last for several years
Proteogylcan content falls, causing cartialge to soften and lose elasticity
Flaking and fibirliiation (vertical clefts) develop along normally smooth articular suface
Cartialge becomes eroded down the subchdonral bone = loss of joint space
Surface changes in cartilage alter distribuiton of biomechnaicl forces and trigger further active changes in tissues
Subchondral bone: eburnation (manifests as subchondral sclerosis on X rays)
vascualr invasion and increased cellularity
Become thickened
Denser at areas of pressure
Traumatised subchondral bone = cystic degeneration to form subchondral bone cysts
Osseous necrosis secondary to chronic impaction (pressure) or to intrusion of synovial fluid
Areas along articular margin, osseous metaplasia of CT occurs = irregular outgrowth of new bone (osteophytes)
OA - symptoms
Deep aching joint pain, exacerbated by use
Reduce range of motion and crepitus (grinding)
Stiffness during rest - morning stiffness <1 hour
Joint stiffness
Pain in hip, gluteal, and groin regions radiating to the knee via obturator nerve
Mechanical pain - accentuated by mobilisation or weight bearing
Crepitus - grating sound or crunching/crackling sensation on movement of joint
Reduced mobility
OA on an xX ray - 4 signs
JOBS Reudced joint space Subchonrdal scleoriss Bone cysts Osteophytes
what is primary OA
Unknown cause
Risk factors- age, Female, ehtnicity (african-american, american indican, hispanic), FH, Nuttirion (high vit C and E some protection against OA)
what is secondary OA
known precipitating cause
obesity
Trauma - sports and occuptaitonal risk factors
Malalignment e.g. developemtn of dysplasia of hip
Infection - septic arthritis, TB
Inflammatroy arthritis -RA, ankylosing spondylitis
Metabolic disroders affecting joints - gout
Haematolgical disorders e.g. haemophilia with haemarthrosis - bleeding into joints
Endocrine abnromalities - Diabetes with neurovascualr impairment - can lead to chronic malaginment of articular surfaces (charcot joint)
OA treatment
Weight reudction if overweight
Activity modification - avoid that precipiate symtpoms
Walking aid
Muscle strenghthening exercises
Orthotic footwear can reablacne a misalined load through a joint
Analgesia (paracetamol) and anti-inflammatories (NSAIDs, COX-2 inhibitors)
Nutritional supplements - glucosamine and chondrotin sulfate
Steroid injections - reduce swelling, alleviate shoulder stiffness and pain
Hyaluroninc acid injections into joint - viscosupplementation - may increase lubrication and possibly promote cartilage repair (evidence is limiting)
Total hip replacemnt = cure
Replaces damaged surfaces with implants and helps to relieve pain and restore mobility
Fracture of femoral neck - what does leg look like
If fracture is displaced, affected leg: shortened, abducted and externally rotated.
Exacerbation of pain on palpation of greater trochanter and pain is exacerbated by rotation of the hip
what happens in an intracapsular fracture
Weight reudction if overweight
Activity modification - avoid that precipiate symtpoms
Walking aid
Muscle strenghthening exercises
Orthotic footwear can reablacne a misalined load through a joint
Analgesia (paracetamol) and anti-inflammatories (NSAIDs, COX-2 inhibitors)
Nutritional supplements - glucosamine and chondrotin sulfate
Steroid injections - reduce swelling, alleviate shoulder stiffness and pain
Hyaluroninc acid injections into joint - viscosupplementation - may increase lubrication and possibly promote cartilage repair (evidence is limiting)
Total hip replacemnt = cure
Replaces damaged surfaces with implants and helps to relieve pain and restore mobility
Intracapsular fracture - treatment
Treated by surgical replacement of femoral head - hemiarthroplasty (femoral head only) or total hip replacement (head and acetabular cup)
Intracapsular fracture - risks factors
Elderly - postmenapasual women with osteoporotic bone
Minor fall
describe extracapsular fracture
Extracapsular - retinacular arterial supply to femoral head likely to remain intact
- Intertrochanteric - Subtrochanteric - Affect young and middle aged population
Sign tramuatic force - RTC
dislocation of hip
Head of femur being fully displaced out of cup-shaped acetabulum of pelvis
May be congenital
Developmental dysplasia of hip (DDH) / congenital dislocation of the hip (CDH)
May be traumatic - severe injury in 16-40 year old in high speed RTCs. Lots of force needed to dislocate normal hip
90% of dislocations = posterior
Posterior dislocation of hip - what does limb look like
shortened, and held in positon of flexion, adduction and internal (medial) rotation
Sciatic nerve palsy - 8-20% cases
Anterior dislocation of hip - limb look like and potential risk
Limb is held in a position of external rotation, Abduction with slight flexion
Femoral nerve palsies can be present , but are uncommon
Describe central dislocation
Central dislocation
Head of femur is driven into pelvis through acetabulum
Always a fracture-dislocation
Femoral head is palpable on rectal examination - high risk of intrapelvic haemorrhage due to disruption of pelvic venous plexuses
Can be life threatening injury
Femoral neck fracture
High velocity trauma - falls from a height, or RTC.
Proximal fragment is abduacted due to pull of gluteus medius and maximus on greater trochanter and flexed due to action of iliopsoas on lesser trochanter
Distal segment is adducted into a varus deformity due to action of adductor muscles (adductor magnus, gracilis) and extended due to pull of gastrocnemius on posterior femur
Patient: tense swollen thigh
Femoral neck fracture - complications
Blood loss in closed femoral shaft fracutres: 1000-1500mL and pateint may develop hypovalaemic shock
Blood close in open femoral shaft fractures: may be double
Complications due to invovlement of neighbourin neurovascualr structures within fracture site are rare
Femoral neck fracture - treatment
surgical fixation
Femoral neck fracture -risk factors
Young children: non-accidental injury (child abuse) should be considered
Elderly with osteoporotic bones or patents with bone metastases or other bone lesions (bone cysts), can occur following a low velocity injury i.e. falling over from standing position
Distal Femoral Fractures
Young patients: high energy sporting injury, sig displacement of fracture fragments. Pic below you can see unfused epihyses in proximal tibia
Elderly: assocation with osteoporotic bone, fall from stanidng
Popliteal artery may beocme invovled if there is sig displacement of fracture
Careful assessment of neurovascular status of limb before, and after, reduction of fracture is essnetial
Tibial platateu fracture
High energy injuries
Axial (top to bottom) loading with varus or valgus angulation (an abnormal medial or lateral flexion load) of the knee
Asoscaited with meniscal tears and ACL injuries
Fractures affecting articulating surface of tibia within the knee joint
○ Unicondylar - affecting one condyle
○ Bicondylar - affecting both tibial condyles
○ Affecting lateral tibial condyle most common
Articular cartialge is always damaged
Most patients will develop a degree of post traumatic osteoarhritis in affected joint
Patella fracture- cause
1% of all skeletal injuries
Direct impact injury - knee against dashboard
Eccentrci conctraction of the quadriceps (muscle is contracting but joint is extending)
Age 20-50 years
Patella Fracture - examination and blood supply
Most important blood supply is via inferior pole
Examination: palpable defect in patella and haemarthrosis (blood in joint)
If extensor mechanism is disrupted (fracture completely splits the patella distal to insertion of quadriceps tendon), patient will be unable to perform a straight leg raise (keep knee extending and flexing at hip)
Patella Fracture - treatment
Reqire reduction an surgical fixation
Undisposed patellar fracutres: protected whilst healing takes palce through splingitn and using crutches, do not usually require surgical fixation
8% of population the patella is bipartite (2 parts) and can be mistaken for a patella fracture on X ray
Develops because there is failure of union of secondary ossifcation centre with the main body of patella
○ Normal anatomical variant
Patella Dislocation
Patella completely displaced out of its normal alignment
Subluxation is partial displacement
Dislocate laterally
Patella usuall held in correct position by contraction of inferior, almost horizontal, fires of vastus medialis, vastus medialis obliquus (VMO)
Role of VMO - stabilise patella within trochlear groove and to control tracking of patella when knee is flexed and extended
Role of VMO
stabilise patella within trochlear groove and to control tracking of patella when knee is flexed and extended
Patella Dislocation - causes
trauma
Often a twisting injury in slight flexion or a direct blow to the knee
Athletic teenagers
Internal rotation of femur on a planted foot whilst flexing the knee (sudden change of direction during sports)
Factors that can predispose to patellar dislocation
Generaled ligamentous laxity
Weakness of quadricpes msucles, especailly VMOShallow trochlear (patellafemoral) groove with a flat lateral lip
Long patellar ligament
Previous dislocations
Patella Dislocation- treatment
extending knee then manually reducing the patella.
Imbolisation used whilst healing takes place
Followed by physiotherapy to strengthen VMO
Menisci tear
Most common type of knee injury
Sudden twisitng motion of a weight bearing knee in high degree of flexion
Intermitten pain, localised to joint line, knee clicking, catching, locking (inability to fully extend the knee due to an intra-articualar foreign body) or a sensation of giving way
Meniscal tears that result from chronic degenerative process within knee have simialr prognosis wit ocnservative magaesment as with surgery
Menisci tear - examination
Exmaination: patient has joint line tenderness and restricted motion due to pain/swelling.
Mechnanical blod to motion or locking can occut with a dispalced tear due to loose meniscal fragments becoming trapped between articular surface
Menisci tear - treatment
Acute traumatic meniscal tears treated surgically
Meniscetomy or meniscal repair
Menisci tear - symptoms
Swelling - delayed symtpom due to a reactive effusion or not at all
As menisci are largely avascualr (except at periphery)
Acute haemarthrossi is rare and if present = tear in peripheral vascular aspect of meniscus or an associated injury to anterior cruciate ligament (ACL)
Chronic effusion (increased synovial fluid) can occur due to synoitis - inflammation of synvoial membrane
Collateral Ligament injury
Sporting injury - direct contact sports like football
Acute varus or valgus angulation of knee
Medial and lateral collateral ligaments noramlly control lateral movement of knee joint and brace it against unusual varus or valgus deformation
Collateral ligaments + posterior cruciate ligament (PCL) to prevent excessie posterior motion of tibia on the femur
What is varus
medial angulation of distal segment
what is valgus
lateral angulation of distal segment
vaLgus = Lateral
Acute valgus strain
Valgus: Medial collateral ligament (MCL) is at risk
In Varus strain: Lateral collateral ligament (LCL) is at risk
MCL - injuryed more commonly than LCL, but a torn LCL has a higher change of causing knee instability
Medial tibial plateau forms a deeper and more stable socket for the femoral condyle than lateral tibial plateua
§ An intact LCL plays a more ciricial role in maintianing staiblity of knee
- Patient will expereince pain and swelling of knee
- As initial pain and stiffness subside, knee joint may feel unstable and patient may complain of it giving way or not supporting their body weight
Unhappy triad
Blown knee
Injury to:
ACL, MCL and medial meniscus
Strong froce applied to lateral aspect of knee
Medial meniscus is firmly adherent to MCL
Cruciate ligament injury - test
Lachmans test
Patient supine on table,
injured kee flexed at 20C to 30 C, hold atients thigh with one hand, place other hand beneath the tibia with thumb of that hand on tibial joint line
pull forward on tibia, firm resistance = unharmed ACL
ACL injury
Weaker than PCL, more common to be injured
Quick deceleration, hyperextension or rotational injury
Non-contact injury aka no other players involved
Popping ensation in knees + immediate swelling
Instability of knee
Knee gives way – tibia slides anterior under femur
anterolasteral rotatory instability, with tibia rotating medially (interanally) during flexion of knee and opening-up laterally
Athletes- surgery
Test: Lachman’s test
PCL injury
Dashboard injury
Knee is flexed and large force is applied to upper tibia, displacing it posteriorly.
RTCs
During football when player falls on flexed knee with ankle plantarflexed
Severe hyperextension injury
Conservative management with bracing and rehab
Knee dislocation
uncommon injury and always results from high energy trauma.
at least three of the four ligaments (MCL, LCL, ACL and PCL) must be ruptured.
An associated arterial injury is very common because the popliteal artery is tethered proximally when it enters the popliteal fossa at the adductor hiatus and distally where it exits the popliteal fossa by passing under the tendinous arch of the soleus muscle
As the popliteal artery is so immobile, if the knee joint dislocates, there is a high risk of it being injured.
It may tear resulting in an obvious haematoma
it may be crushed or suffer a traction injury (with endothelial damage leading to subsequent thrombotic occlusion; see Virchow’s triad)
After reduction of the knee joint, it is therefore essential to fully assess the vascularity of the leg e.g. with Magnetic Resonance Angiography (MRA).
Knee effusions
An effusion is an accumulation of fluid inside the knee joint
Acute (defined as < 6 hours after injury e.g. after cruciate ligament rupture)
- delayed (> 6 hours after injury). In an ACL rupture, bleeding often occurs inside the joint; this is referred to as a haemarthrosis. Delayed swelling of the knee (e.g. the day after injury) is usually due to reactive synovitis. Inflammation of the synovium, in response to injury, leads to the production of an increased volume of synovial fluid.
what is a haemarthrosis
ACL rupture until poven otherwise
Acute knee effusion
Lipo-haemarthrosis
Blood and fat in joint
fracture until proven otherwise as the fat has usually released from the bone marrow.
a fat-fluid interface can be seen on the X-ray
Fat is less dense tLihan blood, absorbs fewer X-rays and therefore appears darker than blood on the X-ray film.
In this X-ray, there is a tibial plateau fracture; it is difficult to see on the X-ray but the presence of a lipohaemarthrosis gives the radiologist a strong indication that a fracture is present.
Housemaids knee
Pre patellar Knee pain and swelling Erythema overlying inflamed bursa Cant kneel on affected side History of a fall onto knee/blunt trauma to knee
Clergyman’s knee
2 bursae – Superficial (patella tendon and skin) and deep (patella tendon and tibia bone)
Affects superficial mostly
Repeated microtrauma caused by activities involving kneeling.
Suprapatellar bursitis & Knee effusion
Suprapatellar bursa is an extension of synovial cavity of knee joint – knee effusion presents with swelling in suprapatellar pouch (the suprapatellar bursa extends superiorly from beneath the patella under the quadriceps muscle)
Causes of knee effusion
OA Rheumatoid arthritis RA Infection (septic arthritis) Gout and pseudogout Repetitive microtrauma to the joint (as a result of running on soft or uneven surfaces)
Semimembranous/popliteal cysts/baker’s cyst
Swelling in popliteal fossa
Fluid is the semimembranosus bursa is an indirect consequence of swelling within the knee joint
Located beneath deep fascia of popliteal fossa in interval between semimembranosus muscle and medial head of gastrocnemius muscle
If the knee joint is inflamed and there is an effusion, the fluid can force its way through this narrow communication into the semimembranosus bursa.
Osgood-Schaltter’s disease (OSD)
inflammation of the apophysis (site of insertion) of the patellar ligament into the tibial tuberosity.
occurs in teenagers who play sport (running and jumping)
OSD treatment
: rest and ice. The pain and swelling resolve at the age of skeletal maturity when the apophysis (which has a separate ossification centre) fuses.
However, the bony prominence usually remains permanently
OSD symptoms
causes localised pain and swelling.
It is bilateral in 20-30% of cases aka mainly unilateral
Patients complain of intense knee pain during running, jumping, squatting, ascending and descending stairs and during kneeling.
OA of knee
knee pain, stiffness and swelling.
The pain may follow a pattern, for example:
Knee pain that comes and goes, possibly with a chronic low level of pain punctuated by more severe flare-ups
Pain precipitated by activities such as bending, kneeling, squatting or climbing stairs
Pain and stiffness that is worse after prolonged inactivity or rest, such as getting out of bed in the morning.
Loss of articular cartilage leads to friction as bone rubs on bone during movement.
This increased friction can be felt as crepitus (a grating sound and crackling sensation on movement of the joint).
An effusion may develop and the swelling further limits joint movement.
OA risk factors
- age,
- female sex,
previous trauma to the joint,
obesity,
family history of OA,
- female sex,
having another condition that has affected the joint (e.g. rheumatoid arthritis, gout, septic arthritis, haemophilia with haemarthrosis)
OA treatment
Initially patients are taught strengthening exercises to strengthen the vastus medialis muscle and therefore reduce instability.
Analgesia, weight loss (if overweight) and activity modification are also used initially.
many patients will require surgery in the form of a total knee replacement (TKR).
Septic arthristis
invasion of jint space by microbes (usually bacteria, but virsues, mycobacteria and fungi too)
e.g. Staphylococcus aureus
Staph. Epidermidis (produces a biofilm), Neisseria gonorrhoeae (in sexually active individuals), Strep. viridans, Strep. pneumoniae and the Group B Streptococci
Reactive arthritis
sterile inflammatory process that can result from an extra-articular infection e.g. gastroenteritis
Risk factors for Septic arthritis of knee
the extremes of age diabetes mellitus, rheumatoid arthritis, Immunosuppression intravenous drug abuse.
prosthetic joints at septic arthritis
- Prosthetic joints (joint replacements) are particularly at risk, either due to intraoperative contamination (60-80% of cases), or to haematogenous spread from a distant infective focus (e.g. during dental surgery). The patient may become symptomatic months or even years after the initial operation. Delayed wound healing is a major risk factor for prosthetic joint infection. The biofilm produced by Staph. epidermidis protects this pathogen from the host’s defences and from antibiotics.
Polymethacrylate cement used in the joint replacement also inhibits white blood cell and complement function, thereby increasing the risk of infection.
Septic arthritis symptoms
Triad
Fever (40-60% of cases)
Pain (75%)
Reduced range of motion.
Treatment for septic arthritis
aspiration of the joint should be carried out immediately and the aspirate should be sent for urgent microscopy, culture and sensitivities.
Compartment syndrome - clinical signs
Severe pain in limb excessive for degree of injury
Increasing and not relieved by analgeisa
Pain exacerbated by passive stretch of muscles
Compartment syndrome - treatment
fasciotomy - surgical decompression of al affected compartments
Compartment syndrome - short term consequences
Decreased perfusion of muscle due to increase in intracomparmentla pressure
Ischaemic muscle releases mediators which further increase capillary permeability and exacerbate rise in intracomparmental pressure
Severe untreated cases: rhabdomylsosis (muscle necrosis) and acute kidney injury
Neurovascular signs develop late - undeveloped at time of diagnosis
Compartmental pressure > systolic arterial pressure = loss of peripheral pulses and increased capillary refill time
Nerve fibres are susceptible to ischaemia - thin cutaneous nerve fibres affected more quickly than motor fibres
Distal paraesthesia preceds loss of motor function
Compartment syndrome - long term consequences
Rhabdomylolysis
Acute kidney injury
Volkamnn’s ishcaemic contracture (nectoric muscle undergo fibrosis)
Permamnt painful an disabling contracture of affected muscle group
Ankle fractures
Inversion or eversion injury
consider co-morbidites as affect healing (e.g. DM double healing time)
Fracture blisters
Common after ankle fractures
Surgery delayed until blisters healed
Skin over fracture blister may become necrotic = healing takes v.long
Open ankle fractures
- Skin barrier is breached and direct communication between fracture and external environment
Common
Urgent surgery with extensive irrigation and debridement to reduce risk of osteomyelitis (infection of bone)
Ankle joint and associated ligaments can be visualized as a ring in coronal plane
The proximal part of the ring is formed by the articular surfaces of the tibia and fibula, united at the inferior tibiofibular joint by syndesmotic ligaments.
The medial side of the ring is formed by the medial (deltoid) ligament
The inferior part of the ring is formed by the subtalar joint (between the talus and the calcaneus).
The lateral side of the ring is formed by the lateral ligament complex of the ankle (anterior talofibular, talocalcaneal and posterior talofibular)
Talar shift
Disruption of any 2 of the syndesmosis, medial or lateral ligaments, ankle motrise becomes unstable and widens = talus can shift medially/laterally
Pic - fractured lateral malleolus and torn deltoid ligament, talor shift
Stable ankle fracture treatment
Non-operativeair cast boot fibreglass cast for comfort Weight bear safelyLow rate complications - i.e. secondary OA
Unstable ankle fracture
Surgical stabilisationhigh risk surgery (DM or peripheral vascular disease
Sprained ankle
partial or complete tear of one or more ligaments of ankle joint
Excessive strain on ligaments of ankle = excessive external rotation, inversion or eversion of foot due to external force
When foot is forced past its normal range of motion, excess stress puts a strain on ligaments
If strain is great enough to pull a ligament past its yield point = damaged ligament or ‘sprained’
90% heal with rest and time
10% that don’t heal = late ankle instability, surgery maybe
Sprained ankle risk factors
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.
Achilles tendon rupture
Men aged 30-50 years during recreational sports ‘weekend warriors’ bursts of jumping, pivorting, and running
Making a forceful push off with an extended knee - i.e. jumping
Fall with foot outstretched in front and ankle dosriflexed, forcibley overstretching tendon Falling from a height, or abruptyly stepping into a hole or off a kerb
Achilles tendon rupture - site of rupture
vascular watershed area. 6cm proximal to insertion of Achilles tendon (calcaneal tendon) onto the calacenal tuberosity)
Area of decreased vascularity and thickness of tendon = therefore more susceptible to tearing
Achilles tendon rupture - symptoms and signs
Sudden and severe pain at back of ankle or in calf (kicked in heel)
Sound of a loud pop or snap
Palpable (sometimes visible) gap or depression in tendon
Intital pain and swelling followed by bruising
Inability to stand on tip toe or to push off whilst walking
Test for achilles tendon rupture
Thrompsons/Simmod’s test
Squeeze calf, normal resonse floot plantar flexes
Rupture: no/reduced movement
Achilles tendon rupture treatment
Conservatitliy with foot being held in correct position in an aircast boot
Surgery has high complication rate
5-10% : wound complications because overlying skin is thin and poorly vascularised
Re-reputure rate of 2-8% after surgery with a similar rate post conservative management
Bunions
Hallux Valgus
Varus deviation of 1st metatarsal
Valgus deviation and/or laterla rotation of hallux
Prominence of 1st metarsal head, with or without an overylign callus
Bunions - risk factors
Most common in middle aged F
Painful movement of 1st MTPJ and difficult with footwear
Most comon cause of a ‘bunion’ = bony deformity at 1st MTPJ
High heels or tight ditting shoes do not cause hallux valgus but can excacerabit it if already present
Occur secondary to trauma, arthtriyc/metabolic conditions ie. gout, RA< psoriatic arthrisis and to CT disorders such as ligamentous laxity (Ehler’s Dnlos syndrome)
Bunions - treatment
Surgery not recommended for cosmetic reasons - convert a painless foot into a painful foot
Surgery- metatrsal oseomoty (cutting throgu metatarsal bone) and realingn the fragments
May also needed to be done in proximal phalanx of great toe
OA of foot and ankle
Hallux rigidus
OA of 1st MTPJ = stiffness of joint
Causes: tremendous stress during walking, each step a force = 2x body weight passes through this joint
Secondary causes: gout and previous septic arthritis
Range of dorsiflexion of toe becomes severely restircted due to arthritis
Plantar flexion retained
Dorsal bunion (osteophyte) may develop on top of joint and rub on patients shoe
OA of foot and ankle symptoms
Pain in MTPJ on walking and attempted dorsiflexion of toe
Severe cases: pain may be present at rest
Patients compensate by walking on the outside of their foot (inversting the foot and walking on lateral border)
OA of ankle joint
All cases are secondary arthritis
Other risk factors: joint stress (ballet dancers, footballers) and obesity
OA of foot Treatment
Activity modification, analgesia, orthotics or aids and sometime intra-articular steroid injections
Rigid sole orthotic = v.stiff shoe insert that prevents motion at 1st MTPJ, help prevent pain caused by dorsiflexion of toe whilst walking
Surgery may be considered if conservative management fails
Gold standard treatment: arthrodesis (fusion) of 1st MTPJ
Join is excised so that it is effectively replaced by a ‘fracture’
‘fracture’ is then stabilised with screws and then normal fracture healing subsequently fuses the joint
Arthroplasty (replacement) of 1st MTPJ may be considered
Post traumatic arthritis
70-80% of cases
Joint previously suffered trauma - fracture, severe sprain
Initially, may heal with full return of ankle function, some cases, subsequent development of OA = further symptoms within couple of years of injury/ delayed for decades
Primary ankle arthritis
7% of cases
No identifiable precipaiting causes
OA foot treatment
Gold standard = arthrodesis (fusion). Very good outcome. Can walk v.well and have mobility of mid foot and fore-foot. No discernbile limp
Alternatively: ankle arthroplasty (joint replacement) - mor emajor operation that carries risk (prostehtic loosening and prosthetic infection)
Achilles tendinopathy
Denegative not inflmamtory process
Tendinopathy can develop
Point of insertion of Achilles tendon into calcaenum = insertional tendinopathy
Vascular ‘watershed’ area within the Achilles tendon = non-insertional tendinopathy
Achilles tendinopath - symptoms and signs
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): see X-ray opposite
Achilles tendinopathy treatment
Physiotherapy
Eccentric stretching exercise to try and improve vascularity of tendon and promote healing
Claw toe
- Affects all 4 of small toes at same time
Toes are hyperextended at MTPJ and flexed at PIPJ (sometimes at DIP joint too so toe curls under foot)
Corns may develop over dorsum of toe or under head of metatarsal
Muscle imbalance = ligaments and tendons to become unnaturally tight = neurological damage and may be secondary to conditions ie. cerbral palsy, stroke, DM, alcohol dependend e
Trauma, inflmaaiton and RA
Hammer toe and mallet toe
Second toe mainly affected
Hammer toe: toe is flexed at PIPJ
Mallet toe: flexed at DIPJ
Causes: ill fiting potinted shoes, pressure on 2nd toe from an adjacent hallux valgus
Tight shoe casues a toe to stay in flexed postion for too long - muscles contract and shorten. Harder to extend toe. Over time, muscles cannot extend the toe
Curly toes
Congenital 3rd-5th digits Bilateral FH of curly toes Develop because tendons of FDL or FDB are too tight Asymptomatic
Treatment: conservation with passive extension of toes and stretching of flexor tendons. Surgery is rarely needed and only considered after age 6 if causes pain on activity
pes planovalgus
Flat foot
Medial arch of foot has collapsed so that medial border fo foot almost touches the ground
Valgus = valgus angulaton of hindfoot
Most young children appear flat footed as arches have not developed and large amount of subcutaneous adipose tissue in sole of foot = medial fat pad
= medial longitnitudal arch of foot begins to form aged 5.
- If deformity persisits into aldolescen or recurs during/after adolescne = abnormal
Orthotics are ineffective in promoting normal developemet of arch and should not be prescribed
Flexible flat feet
No medial arch whilst standing normally, but when standing on tip-toes, normal medial arch appears and hindfoot returns from valgu devaition into a noraml alignment
Rigid flat feet = abnormal
Develop as a result of tarsal coalition (failure of tarsal bone to separate during embryonic development)
Stand on tip toes, no arch appears and hindfoot remains valgus
Adult acquired flatfoot
Dysfucntion of tibilais postrior tendon (usually supports medial long arch of foot whislt walking)
Middle aged F - give a history of a change in shape of their foot and often describe pain behind the medial malleoluls
Risk factors: obesity, hypertension and diabetes
Occur temporailtiy during preganncy, due to increased laxity of ligaments
Stretching of spring ligament (plantar calcaenovasciualr ligament) and plantar aponeurosis
Stretching = talar head being displaced inferomedially, flattening the medial longitudinal arch and producing lateral deviation of hindfoot
Adult acquired flatfoot treatment
Orthtotics (insoles) = 80% improvements to support medial arch
Physiotherahpy to improve muscle strength
Surgical reconstrction
If Seconadry OA has develoepd, arthrodesis of joints of their hindfoot
DM foot
DM foot
infection, ulceration or destruction of tissues of foot
A combination of the 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. Because there is a loss of protective sensation, the patients will often continue to weight-bear on very significant soft tissue abnormalities, thereby exacerbating the problem.
To reduce the risk of foot disease, patients with diabetes attend regular ‘diabetic foot clinics’ for screening.
Their feet will be checked for any corns, callouses, cracks and dry skin. Sensation and perfusion of the feet are assessed and their shoes are checked to make sure that they are suitably protective against trauma (strong soles, not open-toed) and that they fit well (e.g. are not rubbing).
Patients are educated on how to look after their feet and reduce the chance of complications.
Tight glycaemic control is also emphasised as being important in preventing the development of neuropathy and vascular disease and in maintaining a healthy immune response
Charcot arthropathy
Poorly controlled diabest
Progresive destructionof bones, joonts and soft tissues
Ankle and foot but can affect other joints- ie. knee
Neuropathy, abnormal loading of foot, repeated microtruama (with non-healing microfractures) and metabolic abnromalties leads to inflammation causing osteolysis (bone resoprtion), fractures, dislocation and deformity
Patient has reduced ability to detect touch, temp and pain, thus continous to walk on Charcot foot = making injury worse
Neuropathy leads to msucle spasticify (tight achilles tnedon) = exacerbates the deformity
Rocker-bototom foot may develop
Charcot arthropathy treatment
optimisation of glycaemic control
reduction of the load placed on the affected joints. However, this can be challenging as there is reduced bone stock and the bones are soft (due to inflammation).
The patients often do not experience pain, so are not reminded to stop weight-bearing on the foot.
They are also often obese which increases the load placed through their softened bones; and they usually have poor glycaemic control and therefore have secondary immunosuppression.
