musculoskeletal Flashcards
what is bone?
specialised form of connective tissue
unique histological
composition allows it to carry out numerous functions
what are the 5 functions of bone?
support
protection
locomotion
haematopoiesis
lipid and mineral storage
what is the function of bone in terms of support?
framework and shape of the body
what is the function of bone in terms of protection?
surrounds major internal organs and vasculature
what is the function of bone in terms of locomotion?
joints to allow flexibility and attachment site of muscles
what is the function of bone in terms of haematopoeisis?
reservoir of stem cells forming blood cells
what is the function of bone in terms of lipid and mineral storage?
adipose tissue stored within bone marrow
calcium stored within hydroxyapatite crystals
what are the 5 types of bone?
flat
long
short
irregular
sesamoid
what is the function of flat bones?
protect internal
organs
what are some examples of flat bones?
skull
thoracic cage
sternum
scapula
what is the function of long bones?
support and facilitate
movement
what are some examples of long bones?
humerus
radius
ulna
metacarpals
what is the function of short bones?
provide stability and some movement
how can a short bone be described?
no diaphysis, as wide
as they are long
what are some examples of short bones?
carpals
tarsals
how can irregular bones be described?
vary in shape and
structure
what are some examples of irregular bones?
vertebrae
sacrum
pelvis – pubic, ilium
or ischium
where are sesamoid bones found?
embedded within tendons
what is the function of sesamoid bones?
potentially protect tendons from stress or wear
what are some examples of sesamoid bones?
patella
how can a long bone be divided up?
epiphysis
metaphysis -
what is the epiphysis?
rounded end of bone, found at joint with adjacent bone
area of long bone where bone growth takes place from
how does the epiphysis grow?
grow from the epiphyseal plate and push new bone outward
ossifies separately
what is the structure of the epiphysis?
spongy (cancellous) bone
layers of compact (cortical) bone around it
what is the metaphysis?
neck portion of a long bone between the epiphysis and the diaphysis
contains the growth plate
what is the function of the metaphysis?
transfer loads from weight-bearing joint surfaces to the diaphysis
what is the epiphyseal line?
epiphyseal plate that has ossified
divides diaphysis and epiphysis
what is the periosteum?
membrane on outer surface of long bones
covers all except areas surrounded by cartilage and where tendons and ligaments attach
what is the structure of the periosteum?
outer fibrous layer - collagen and reticular fibres
inner proliferative cambial layer
what is the medullary cavity?
central cavity of bone shafts where red bone marrow (in children) and/or yellow bone marrow (adipose tissue) is stored
what is the structure of bone in the diaphysis?
yellow bone marrow in medullary cavity (lined by endosteum)
surrounded by compact (cortical) bone
how can bone ultrastructure be divided into 2 categories?
woven (primary) bone
lamellar (secondary) bone
how can woven (primary) bone be described?
first type of bone to be formed – in embryonic development and fracture healing
consists of osteoid, randomly arranged collagen fibres
temporary structure replaced by mature lamellar bone
how can lamellar (secondary) bone be described?
bone of the adult skeleton
highly organised sheets of mineralised osteoid, making it much stronger than woven bone
how can lamellar (secondary) bone be categorised?
compact (cortical)
spongy (cancellous)
how is cortical (compact) bone structured?
found in the diaphysis, forms the outer part of bone
organised in concentric circles around a vertical Haversian canal
Haversian canal are connected by Volkmann’s canals which contain small vessels that also supply periosteum
osteocytes located between lamellae, within small cavities called lacunae - these
are interconnected by a series of tunnels called canaliculi.
entire structure is known as an osteon, the functional unit of bone
how is cancellous (spongy) bone structured?
found in the epiphysis
irregular crosslinking of trabeculae to form porous yet strong bone resistant against multidirectional lines of force
large spaces between trabeculae giving it a honeycombed appearance
contains red bone marrow
what is the purpose of the extracellular matrix in bone?
provides biomechanical and structural support
what are the components of extracellular matrix in bone?
collagen – Type I (90%) and type V
mineral salts – calcium hydroxyapatite (70% of bone)
when does calcification of bone occur?
mineral salts interpose between collagen fibres
when is the extracellular matrix known as osteoid?
before calcification (before mineral salts interpose between collagen fibres)
what is the function of osteoblasts?
synthesis uncalcified extracellular matrix (osteoid)
i.e. build bone
how are osteocytes formed?
as osteoid mineralizes, osteoblasts are entombed between lamellae, becoming osteocytes
lay down concentric lamellae to form osteons
what is the function of osteocytes?
regulate bone mass by monitoring mineral and protein
content
what are osteoclasts derived from?
monocytes
are multinucleate
what are the functions of osteoclasts?
resorb bone, multinucleate cells
release H+ ions
release lysosomal enzymes
what are osteoprogenitor cells?
undifferentiated stem cells
how does bone’s blood supply compare to that of cartilage?
good compared to cartilage
nutrient arteries supplying diaphysis and meta/epiphyseal vessels
what are the two ways in which bone can grow?
endochondral (appositional)
intramembranous (interstitial)
how does the bone grow (endochondral)?
formation of bone onto a temporary cartilage scaffold (e.g. hyaline cartilage replaced by
osteoblasts secreting osteoid in femur)
provides length
how does the bone grow (intramembranous)?
formation of bone directly onto fibrous connective tissue (e.g. temporal bone or scapula)
provides width
how is bone removed?
via osteoclasts
why is bone removal as part of turnover important?
essential for body’s metabolism
removal of bone increases calcium in blood
how is bone produced?
via osteoblasts
what allows osteoblasts to synthesise bone matrix?
receptors from: - PTH - prostaglandins - vitamin D - cytokines are activated
allows synthesis of bone matrix
how can the co ordinated action of osteoblasts and osteoclasts be described?
cutting cones that essentially drill through old bone
how can osteoporosis be described?
decrease in bone density, reducing
structural integrity
why does osteoporosis occur (referring to bone cells)?
osteoclast activity > osteoblast activity
what are the three types of osteoporosis?
postmenopausal
senile
secondary
what causes rickets (children)?
vitamin D or calcium deficiency in childhood
what causes osteomalacia?
vitamin D or calcium deficiency
what mechanism causes rickets and osteomalacia?
osteoid mineralizes poorly, remains pliable
how does rickets affect epiphyseal growth plates?
can become distorted under body weight
what are the negative consequences of osteomalacia?
increased fracture risk
what causes osteogenesis imperfecta?
rare genetic autosomal dominant inheritance
causes abnormal collagen synthesis
what are the negative consequences of osteogenesis imperfecta?
increased fragility of bones
bone deformities
blue sclera
what can osteogenesis imperfecta be misdiagnosed as and why is this important?
can be mistaken as NAD (non-accidental damage?) in children
diagnosis important medicolegally
what is a fracture?
discontinuity of bone
what are the four ways of describing a fracture?
orientation
location
displacement
skin penetration
what are the four types of fracture orientation?
transverse
oblique
spiral
comminuted
how can a transverse fracture be described?
straight through the width of the bone (90 degrees to bone direction)
how can an oblique fracture be described?
diagonal across bone
how can a spiral fracture be described?
winds around bone
how can a comminuted fracture be described?
break or splinter of the bone into more than two fragments
“spiderweb” appearance
what are the three types of fracture location?
proximal third (epiphysis, metaphysis, beginning of diaphysis)
middle third (middle portion of diaphysis)
distal third (lower portion)
what are the two categories of displacement in a fracture?
undisplaced (fracture ends line up)
displaced (movement of bone, fracture end do not line up)
what are the two categories of skin penetration in a fracture?
open (bone end has gone through skin)
closed (bone end remains within skin)
why are fractures classified?
improve communication of fractures (standardised)
assist with prognosis or treatment
what are some different classification systems of a fracture?
descriptive classification (e.g. Garden, Schatzker, Neer, Wber)
associated soft tissue injury (e.g. Tscherne in closed, Gustilo-Anderson in open)
universal classification (e.g. OTA classification - AO/OTA classification considers the bone, where the fracture is, the type, group and subgroup)
how does primary (direct) bone healing occur?
intramembranous healing, occurs via Haversian remodeling
little (<500mm) or no gap
slow process
cutter cone concept – like bone remodelling
what are the four steps of secondary (indirect) bone healing occur?
haematoma formation
soft callus formation
hard callus formation
remodelling
how does secondary (indirect) bone healing occur?
endochondral healing, involves responses in the periosteum and external soft tissues
fast process resulting in callus formation (fibrocartilage)
what occurs during haematoma formation in secondary (indirect bone healing)?
damaged blood vessels bleed forming a haematoma
neutrophils release cytokines signalling macrophage recruitment
what occurs during soft callus formation in secondary (indirect bone healing)?
collagen and
fibrocartilage bridge the fracture site and new blood vessels form
what occurs during hard callus formation in secondary (indirect bone healing)?
osteoblasts, brought in by new blood vessels, mineralise the
fibrocartilage to produce woven bone (calcified matrix)
what occurs during remodelling in secondary (indirect bone healing)?
months to years after
injury osteoclasts remove woven bone and osteoblasts laid down as ordered lamellar bone
medullary canal re-established
what are the prerequisites for fracture healing?
minimal fracture gap
no movement if direct (primary) bony healing, some movement if indirect
(secondary) bone healing
patient physiological state – nutrients, growth factors, age, diabetic, smoker
what are the usual timeframes for fracture healing?
usually pre-defined timeframe, around 6 months
lower limb fractures take twice as long as upper limb fractures to heal
paediatric fractures heal twice as quickly as adults
what does Wolff’s law state?
bone adapts to forces placed upon it by remodelling and
growing in response to these external stimuli
how should Wolff’s law be applied if a child’s femur heals bent?
axial loading should be direct, with
remodelling occurring through axial loading
periosteum on the concave side will make more bone while on the convex
side, bone will be resorbed
what are the six types of fracture healing complication?
malunion
atrophic non-union
oligotrophic non-union
hypertrophic non-union (horse hoof)
hypertrophic non-union (elephant foot)
pseudoarthrosis
what is a fracture malunion?
bone healing occurs but outside of the normal parameters of
alignment (i.e. ends don’t line up)
what is a fracture non-union?
failure of bone healing within an expected time frame
what is an atrophic non-union in fracture healing?
healing completely
stopped with no XR changes, often physiological
caused by inadequate immobilization and inadequate blood supply
what is a hypertrophic non-union in fracture healing?
too much movement, causing callus healing
caused by inadequate stability with adequate blood supply and biology
abundant callous formation without bridging bone
what are the four R’s in fracture management?
resuscitate - save the patients life, then worry about the fracture
reduce – bring the bone back together in an acceptable alignment
rest/restrict – maintain reduction to prevent distortion or movement, provide stability
rehabilitate - get function back and avoid stiffness (use, move, strengthen, weight bear)
what three things should be considered when assessing period of immobility in fracture healing?
functional limitations and support needed
wider MDT
thromboembolism prophylaxis
what are three forms of conservative fracture management?
rest, ice, elevation
plaster/fibreglass cast or splint
traction - skin/bone
what are some forms of surgical fracture management?
external fixation
- mono/biplanar
- multiplanar - ring
arthroplasty
- hemiarthroplasty
- total joint replacement
ORIF (open reduction internal fixation) - open leg and move bone into optimal healing position using screws, rods etc.
intramedullary nail
MUA + K-wire (manipulation under anaesthetic and Kirschner wire) - bones moved into optimal healing position and (if unstable) wires are used to keep it in place (otherwise a cast is used)
how is a fracture diagnosed?
history and examination – tenderness/limb
pain/swelling
obtain X-ray of affected region, ensure in at least two
planes
what is a six step approach to orthopaedic x-rays?
projection
patient details
technical adequacy
obvious abnormalities
systematically review the X-ray
summarise
how is projection approached in orthopaedic x-rays?
any assessment of a bone or
joint generally requires at
least two views
for other sites where
fractures may be difficult to detect more than two views may be needed e.g. scaphoid
how are patient details approached in orthopaedic x-rays?
always check you are looking at the
correct X-ray for the correct patient
double check as often names can be
similar and correlate with DOB and
NHS/Hospital number
state the name, age, and date X-ray was
taken
how is technical adequacy approached in orthopaedic x-rays?
entire area in question should be included
is the exposure adequate to ensure differentiation of soft
tissues and bone?
is there rotation? does it complicate diagnosis?
do you need a full length X-ray or imaging of the joint
above and below?
how are obvious abnormalities approached in orthopaedic x-rays?
is there anything obviously wrong that
stands out?
if there is an obvious abnormality,
comment on it before moving on
is there an obvious fracture, subluxation
or dislocation? can you see a bone lesion?
how is a systematic review of x-ray approached in orthopaedic x-rays?
look around all edges of bones – should be smooth, any
disruption could represent a fracture
look at medulla for disruption to trabeculae or lines of lucency/sclerosis
assess for soft tissue swelling or joint effusions which
could be indirect evidence of fractures
look at joint surfaces for any evidence of subluxation or
dislocation
look at bone density and assess for degenerative changes
how is a summary approached in orthopaedic x-rays?
state key findings
describe fracture
suggest further investigations or management
what is the presentation of a shoulder dislocation?
variable history but often direct trauma
pain
restricted movement
loss of normal shoulder contour
what clinical examination should be done for a shoulder dislocation?
assess neurovascular status – axillary nerve
what investigations should be done for a shoulder dislocation?
X-ray prior to any manipulation – identify fracture e.g. humeral neck, greater tuberosity avulsion or glenoid
scapular-Y view/modified axillary in addition to AP (anterior-posterior)
what are the three types of shoulder dislocation?
anterior
posterior
inferior
how is an anterior shoulder dislocation described?
commonest type (~90%)
bimodal distribution
humeral head not overlying glenoid
how is an posterior shoulder dislocation described?
rare (~6%)
associated with seizures/shocks
‘lightbulb sign’ on x-ray
how is an inferior shoulder dislocation described?
rare (<2-4%)
arm held abducted above head
humeral head not articulating correctly
how is a shoulder dislocation management undertaken?
( avoid vigorous or twisting manipulation
to avoid fractures)
safest method is to use traction-counter traction +/- gentle internal rotation to disimpact humeral head
ensure adequate patient relaxation – Entonox; benzodiazepines
if alone could use Stimson method
undertake in safe environment, especially in elderly e.g. resus, ask
for senior/anaesthetic support early on if necessary
what are some complications of shoulder dislocation?
neurovascular
damage to labrum and/or glenoid
damage to humeral head
recurrent dislocation
how can neurovascular complications of shoulder dislocation occur?
at time of presentation due to trauma sustained e.g. axillary nerve injury
iatrogenic as a result of reduction manoeuvre
delayed onset due to an evolving haematoma post injury/manipulation
how can damage to the labrum and/or glenoid occur as a complication of shoulder dislocation?
Bankart lesion – soft or bony (inside of head)
how can damage to the humeral head occur as a complication of shoulder dislocation?
Hill-Sachs lesion (outer edge of head)
how can recurrent dislocations occur as a complication of shoulder dislocation?
lifetime risk increases i.e. younger the patient, the greater the risk of repeat dislocation
what is the presentation of a proximal humerus fracture?
fall onto an outstretched hand
typically in the elderly or those with osteoporosis
what investigations should be done for a proximal humerus fracture?
plain x-rays
CT if concern over articular involvement or high degrees of comminution
how are proximal humerus fractures classified?
described by Neer
2 part - surgical neck fractures, avulsion fractures of greater tuberosity
comminuted fractures (>3 parts)
how is a 2 part proximal humerus fracture with minimal displacement managed?
collar and cuff
high surgical risk / comorbidities
compliant with post-operative care
how is any proximal humerus fracture with displacement but not highly comminuted managed?
ORIF - plate and screws
how is a humeral head fracture with large displacement treated?
arthroplasty
why is an arthroplasty used to manage a humeral head fracture with large displacement?
high risk of non-union
when is a reverse arthroplasty used (proximal humerus fracture) ?
unrepairable rotator cuff
previous unsuccessful shoulder replacement
complex fracture/chronic shoulder dislocation
what is the presentation of a distal radius fracture?
very common, bimodal distribution
often present with clear mechanism of falling onto affected area, swelling and visible deformity
commonest presentation is dorsal displacement due to fall on outstretched hand
what investigations are done for a distal radius fracture?
plain radiographs
PA/lateral views to assess fracture type
thorough clinical examination to avoid concomitant injuries
what is an extra articular fracture?
break above wrist joint
what are the two types of extra articular fracture?
dorsal angulation - Colles fracture
volar angulation - Smith fracture
what is an intra articular fracture?
break within wrist joint
what are the two types of intra articular fracture?
dorsal angulation - Dorsal Barton
volar angulation - Volar/Reverse Barton
how is a cast/splint used in management of distal radius fractures?
temporary treatment for any distal radius fracture – reduction of fracture and placement into cast until definitive fixation
definitive if minimally displaced, extra
articular fracture
when is an MUA with K wires (manipulation under anaesthetic with Kirschner wires) used in management of distal radius fractures?
for fractures that are extra articular but have instability (particularly in children)
how are K wires removed?
in clinic post-op
when is an ORIF (open reduction internal fixation) used in management of distal radius fractures?
any displaced, unstable fractures
not suitable for K-wires
or with intra-articular involvement
what is the goal of operative management in distal radius fractures?
restore articular surface congruency
radial inclination 22º
radial height 11 mm
volar tilt 11º
what are the eight carpal bones of the wrist?
first row (lateral to medial) - scaphoid, lunate, triquetrum, pisiform
second row (lateral to medial) - trapezium, trapezoid, capitate, hamate
what is the presentation of scaphoid fractures?
commonest carpal bone injury, usually young patients
typically a fall backwards onto their hand, but think in any distal radius
what clinical examinations should be done in scaphoid fractures?
anyone with FOOSH or with distal radius fracture should have scaphoid exam
palpation of anatomical snuffbox, scaphoid tubercle or telescoping of thumb
what investigations should be done in scaphoid fractures?
plain radiographs difficult to assess – request scaphoid views
delayed radiographs if normal but clinical suspicion
consider CT/MRI if still concerned
how is a displaced scaphoid fracture managed?
retrograde blood supply means high risk of non-union/avascular necrosis of proximal pole
most displaced fractures disrupt this and therefore ORIF usually undertaken
how is an undisplaced scaphoid fracture managed?
can be treated conservatively in a scaphoid cast
length of time to heal can be long, some surgeons opt for fixation as a result
what causes perilunate instability?
disruption to any of the ligament complexes
that surround the lunate
what is the difference between perilunate and lunate dislocation?
perilunate - articulation with radius and surrounding carpal bones (scaphoid, triquetrum, capitate and hamate) is maintained
in lunate dislocation it is not
what group of injuries does perilunate dislocation belong to?
perilunate instability
how can a perilunate dislocation be seen on an x-ray?
normal: radius, lunate and capitate in straight line in lateral view
perilunate dislocation: radius and lunate in line with thumb, capitate in line with fingers in lateral view
how can a lunate dislocation be seen on an x-ray?
normal: radius, lunate and capitate in straight line in lateral view
lunate dislocation: radius and capitate in line with fingers in lateral view
what are the four stages of perilunate dislocation?
scapho-lunate dissociation
lunocapitate disruption
lunotriqeutral disruption
lunate dislocation
what occurs in scapho-lunate dissociation (stage 1 of perilunate dislocation)?
widening of scaphoid and lunate due to scapholunate ligament
disruption
what occurs in lunocapitate disruption (stage 2 of perilunate dislocation)?
lunate remains normally aligned with
distal radius, remaining carpal bones
dislocated
capitate and lunate widening
high association with scaphoid fractures
what occurs in lunotriqeutral disruption (stage 3 of perilunate dislocation)?
capitate and lunate are not aligned
with distal radius
lunate-triquestral ligament disrupted
high association with triquetral fractures
what occurs in lunate dislocation (stage 4 of perilunate dislocation)?
dislocation of lunate with a ‘tipped’
teacup’ sign
dorsal radiolunate ligament injury
how is perilunate instability managed non-operatively?
closed reduction and casting has no indication and often poor outcomes compared to non- operative management
high risk of recurrent dislocation
how is acute perilunate instability (< 8 weeks) managed operatively?
ORIF, ligament repair and fixation
good functional outcomes
how is non-acute perilunate instability (> 8 weeks) managed operatively?
proximal row carpectomy (converts wrist into simple hinge type)
how are chronic injuries in perilunate instability managed operatively?
arthodesis of wrist
pain reduction especially if degenerative
what is the presentation of pelvic fractures?
usually a result of high energy trauma
patients can become very unstable – a lot of visceral organs and vasculature are adherent to the pelvis
what examinations are done in pelvic fractures?
ABCDE approach -examine the perineam/urethral opening
digitate – vaginal or rectal examinations – check for visceral damage or bleeding
what investigations are done in pelvic fractures?
plain radiographs
urethrogram
CT +/- angiography
what are the three pelvic fracture classifications?
lateral compression
anterior-posterior compression
vertical shear
how are pelvic fractures managed?
advanced trauma life support (ATLS) and ABCDE principles
address hypovolaemia (common)
definitive treatment via a specialist centre with pelvic surgeons
principle to restore integrity of pelvic ring and alignment of sacroiliac joints
how is the integrity of pelvic ring and alignment of sacroiliac joints restored in pelvic fractures?
internal fixation with plate and screws
external fixation if patient unstable and not suitable for invasive surgery
how is hypovolaemia addressed (in pelvic fractures)?
IV access and resuscitate the patient, think of major haemorrhage protocols early
pelvic binders are use as a tamponade device but need to be placed accurately (over greater trochanters)
ongoing instability should suggest laparotomy or angiographic embolisation
what is the usual cause of a proximal femur/neck of femur fracture in young people?
high energy major trauma
how are proximal femur/neck of femur fractures pathological?
result of osteoporosis and minimal trauma in elderly
what are the general features of a proximal femur/neck of femur fracture history?
often a fairly inconspicuous history of a minor fall
may report groin, thigh or buttock pain
ask about preceding symptoms, always think of pathological causes for a fall (e.g. MI, TIA/stroke, seizure)
ask about comorbidity
pre-injury mobility
social history
what examinations are done for a proximal femur/neck of femur fracture?
MSK – look, feel, move
thorough secondary survey and top-to-toe examination to look for other injuries
what investigations are done for a proximal femur/neck of femur fracture?
plain radiographs
CT if not identified but high suspicion
what is the initial emergency department management for proximal femur/neck of femur fractures?
rule out any other injury/pathology causing fall
involvement of orthogeriatricians/medical team early
pain relief – consider fascia iliaca block in ED if necessary
catheterise – limited mobility
blood tests
ECG/Chest X-ray if >55
pre-operative optimisation – fluids, transfusion?
what is the general guidance for management of patients with suspected proximal femur/neck of femur fractures?
ambulance
- Entonox PRN via mask/mouthpiece
- gain IV access if possible
A&E
- paracetamol +- NSAID
- morphine orally or IV (avoid IM if possible)
- ensure IV route available: start IV fluids 1l NaCl in 10 hrs
- take history
- x-ray
- hourly pain scores (further analgesia if needed)
- if fracture confirmed consider fascia iliaca block, admit to ward give oxygen)
arrival at ward
- pain score, analgesia if needed
- check IV fluids
until surgery and post-op
- 4 hourly pain scores (further analgesia if needed)
- if pain unresolved in 4 hours call pain team
what are the three types of intracapsular fracture?
subcapital (femoral head and neck)
transcervical (midportion of femoral neck)
basicervical (base of femoral neck)
what are the three types of extracapsular fracture?
intertrochanteric (between greater and lesser trochanter)
subtrochanteric (between the lesser trochanter and the femoral isthmus, proximal part of the femoral shaft)
reverse oblique (from lesser trochanteric to lateral edge of femur, parallel to neck)
what are the three types of intracapsular treatment?
total hip arthroplasty
hemiarthroplasty
cannulated screws
what are the two types of extracapsular treatment?
dynamic hip screw
intramedullary nail
what factors are prerequisites for a total hip arthroplasty?
mobile with <1 walking
stick outdoors
no cognitive
impairment
medically suitable for
procedure and
anaesthetic
what factors are prerequisites for a hemiarthroplasty?
mobile with >1
walking stick
outdoors
reduced AMTS (abbreviated mental test score)
comorbidities or
reduced baseline not
benefiting from THR
what factors are prerequisites for cannulated screws?
undisplaced fractures
where vessels unlikely
to be disrupted
young patients
compliant with nonweightbearing while
fracture heals
when is a dynamic hip screw used?
for 2-4 part intertrochanteric fractures
what is the benefit of a dynamic hip screw?
provides compression as prosthesis is perpendicular to fracture line
why are intramedullary nails used?
subtrochanteric
fractures are unstable
due to pull of hip girdle
why are reverse oblique fractures not amenable to dynamic hip screws?
fracture line not perpendicular
what healthcare professionals need to be present for a post-op proximal femur/neck of femur fracture MDT?
geriatrician
physiotherapy
occupational therapy/social worker
what is the role of a geriatrician post-op for proximal femur/neck of femur fracture?
bone health
medical optimisation
secondary fall prevention
what is the role of a physiotherapist post-op for proximal femur/neck of femur fracture?
prevent leading causes of death (HAI, deep vein thrombosis, pulmonary embolism) by early mobilisation
what is the role of an occupational therapist/social worker post-op for proximal femur/neck of femur fracture?
help with post-operative care needs, package of care and assistance or aids at home
why is a femoral shaft fracture concerning?
significant force required to fracture it (largest bone)
high incidence of concomitant life threatening injuries can exist
(assess using ABCDE and advanced trauma life support (ATLS))
what should a clinical examination include in a femoral shaft fracture?
assessment of neurovascular status of affected limb
what x-rays should be taken of a femoral shaft fracture (and any diaphyseal injury)?
x-ray joints above and below to look for fractures or dislocation
what steps are taken for management of a femoral shaft fracture?
resuscitate patients as necessary (hypovolaemia is common as long
bone fractures can bleed a lot)
traction is useful in the first instance as a way of temporarily reducing both pain and bleeding
what are the two operative options for a femoral shaft fracture?
intramedullary nail
ORIF (open reduction and internal fixation)
how is intramedullary nailing used in treatment of a femoral shaft fracture?
can be either antegrade (from the hip) or retrograde (from the knee)
depends on:
- surgeon preference
- injury pattern
- existing prostheses
when is ORIF (open reduction and internal fixation) used in treatment of a femoral shaft fracture?
used if nailing unsuitable (e.g. a segmental
fracture, knee or hip replacements)
why is the proximal tibia important?
key weightbearing surface as part of knee joint, articulating with the distal femur
how can the tibial joint surface be described?
relatively flat
comprises both medial and lateral
plateaus
central tibial spine acting as an insertion point for ligaments
how is a tibial plateau fracture caused?
extreme valgus/varus force or axial loading across the knee
impaction of the femoral condyles causes the
comparatively soft bone of the tibial plateau to depress or split
what injuries are not uncommon with a tibial plateau fracture?
concomitant ligamentous or meniscal injury
what are the three types of lateral tibial plateau fracture?
type 1 - split
type 2 - split and depression
type 3 - depression
what is the one type of medial tibial plateau fracture?
type 4 - medial plateau
what are the two types of medial and lateral tibial plateau fracture?
type 5 - bicondylar
type 6 - metaphyseal-diaphyseal dissociation
what kind of tibial plateau fractures can be managed non-operatively?
only truly undisplaced fractures with good joint line congruency
how can a tibial plateau fracture be assessed for non-operative management?
assessed on CT or
high fidelity imaging
how is a tibial plateau fracture managed operatively?
restoration of articular surface using combination of plate and screws
bone graft or cement may be necessary to prevent further depression after fixation
what is the ankle joint comprised of?
talus articulating with tibia and fibia
what two things provide joint stability necessary for function in the ankle joint?
ligaments
bone projections
which ligaments provide joint stability necessary for function in the ankle joint?
medially: talofibular and calcaneofibular ligaments
laterally: deltoid ligament
which bone projections provide joint stability necessary for function in the ankle joint?
medially: medial malleolus of tibia
laterally: lateral malleolus of fibula
posteriorly: posterior malleolus of tibia
how can an ankle fracture occur?
with twisting or axial
what are two common presenting features of an ankle fracture?
extensive soft tissue swelling
inability to weightbear
what does a clinical examination assess in an ankle fracture?
identify tenderness over ligament complexes
for assessing stability
what does an x-ray assess in an ankle fracture?
to ascertain talar shift
for assessing stability
how are ankle fractures classified?
Weber A-C
what are the features of a Weber A fracture?
occur below the level of the syndesmosis
ligament disruption and joint stability unlikely
what are the features of a Weber B fracture?
occur at the level of
the syndesmosis
ligament
disruption and joint stability possible (stress testing or weightbearing
assessment for talar shift necessary)
what are the features of a Weber C fracture?
occur above the level of the syndesmosis
ligament disruption and
joint instability likely
how is an ankle fracture managed non-operatively?
non-weightbearing below knee cast for 6-8 weeks
can transfer into walking boot
physiotherapy to improve range of motion/stiffness from joint isolation
when is an ankle fracture managed non-operatively?
Weber A (i.e. below syndesmosis and therefore thought to be stable)
Weber B - if no evidence of instability (no medial/posterior malleolus fracture and no talar shift)
when is an ankle fracture managed operatively?
Weber B (unstable fractures – talar shift/medial or posterior malleoli fractures)
Weber C i.e. fibular fracture above the level of the syndesmosis therefore unstable
what does an operative procedure in ankle fracture management require?
soft tissue dependent – patients need strict elevation as injuries often swell considerably
how is an ankle fracture managed operatively?
ORIF (open reduction internal fixation)
with or without syndesmosis repair (using screw or tightrope technique)
syndesmosis screws can be left in situ but may break after some time so therefore can be removed at a later date if necessary
what is a Maisonneuve fracture?
spiral fracture of the proximal third of the fibula
associated with a tear of the distal tibiofibular syndesmosis and the interosseous membrane
what causes a Maisonneuve fracture?
twisting injury disrupts syndesmosis
causes a high fibula fracture
what should be checked for in ankle fractures during clinical examination?
proximal tenderness (Maisonneuve fracture)
patients may have distracting pain of ankle fracture and be unaware
what should be checked if there is widening of the syndesmosis on radiographs but no obvious fibula
fracture?
Maisonneuve fracture – energy has to dissipate
somewhere
what kind of x-rays should be taken for a Maisonneuve fracture?
long length x-rays to visualise the full fibula and ensure no missed fracture
what are the key differences between a child and adult skeleton?
child - 270 bones, continuously changing
physis - one on proximal and distal end of long bones
what are the physis?
growth plates
areas from which long bone growth occurs post-natally
what 2 pathways can bone development be broadly differentiated into?
intramembranous to produce flat bones (cranial bones, clavicle) (mesenchymal cells>bone)
endochondral for long bones (mesenchymal cells > cartilage > bone)
what is the process of intramembranous ossification (flat bones)?
condensation of mesenchymal cells which differentiate into osteoblasts – ossification centre forms
secreted osteoid traps osteoblasts which become osteocytes
trabecular matrix and periosteum form
compact bone develops superficial to cancellous bone - crowded blood vessels condense into red bone marrow
what are primary ossification centres?
sites of pre-natal bone growth through endochondral ossification from the central part of the bone
what are secondary ossification centres?
occurs post-natal after the primary ossification centre
long bones often have several (the physis)
what are the 2 parts of endochondral ossification?
primary ossification - central part of diaphysis (prenatal bone growth)
secondary ossification - physis grow to form long bones (post natal)
what is the process of primary ossification in endochondral bone?
mesenchymal differentiation at primary centre
cartilage model of the future bony skeleton forms
capillaries penetrate cartilage, calcification at the primary ossification centre – spongy bone forms, perichondrium transforms into periosteum
cartilage and chondrocytes continue to grow at ends of the bone
secondary ossification centres develop with own blood
what is the main difference between endochondral and intramembranous ossification?
endochondral involves cartilage before bone
what do the physis contain?
cartilage
how does the epiphyseal side of the physis allow bone elongation?
hyaline cartilage active and dividing to form hyaline cartilage matrix
how does the diaphyseal side of the physis allow bone elongation?
cartilage calcifies and dies, then replaced by bone
what kind of events may impact the growth of a child?
damage to physis
traumatic, infective etc.
what are the 4 main ways in which children’s skeleton differs to that of adults?
more elasticity
physis (i.e. bone growth)
speed of healing (due to continued growth)
remodelling (greater remodelling potential due to growth, can tolerate lots of deformity and angulation)
why are children’s bones more elastic than adults?
increased density of Haversian canals
why do children have increased density of Haversian canals?
bones more metabolically active (continuously growing)
how do children’s bones break differently?
plastic deformity (bends before breaking)
how is a buckle fracture caused?
child may fall onto outstretched hand
instead of the bone fracturing it buckles in on itself
creates Tarus like structure (roman column)
what is a greenstick injury?
(in children)
one side buckles and bends, the other snaps
when does growth stop in children?
growth occurs at varying rates at varying sites
growth stops as the physis closes
what factors affect the closure of the physis?
puberty
menarche in girls
parental height (other genetic factors)
when do the physis close?
girls - 15-16 years
boys - 18-19 years
what can physeal injuries lead to?
growth arrest
growth arrest can lead to deformity (e.g. if only part of the physis cannot grow)
what do the speed of healing and remodelling potential depend on?
location of injury
age of patient (younger child heals quicker as growing more rapidly)
how does the rate of growth vary from physis to physis?
upper limb - around the shoulder and the wrist have faster growth rates
lower limb - knee has faster growth rates (distal femur, proximal tibia)
what are 4 common children’s congenital conditions?
developmental dysplasia of the hip
club foot
achondroplasia
osteogenesis imperfecta
what is developmental dysplasia of the hip (DDH)?
disorder of the neonatal hip
head of the femur is unstable or incongruous in relation to the acetabulum
what causes developmental dysplasia of the hip (DDH)?
occurs when child is in the mother’s womb (“packaging disorder”), usually due to the way that the child sits
affects hip positioning in acetabulum and normal hip development
how does developmental dysplasia of the hip (DDH) affect development of the acetabulum and hip?
acetabulum relies on concentric reduction and balance forces
hip needs to sit within the acetabulum and have the normal forces going through the joint
neither hip nor acetabulum develop properly
what is the spectrum of developmental dysplasia of the hip (DDH) conditions?
dysplasia (most common, 2:100)
subluxation
dislocation (least common, 2:1000)
what is dysplasia in developmental dysplasia of the hip (DDH)?
hip may be within the socket, but not centrally placed
socket does not develop into cup
what is subluxation in developmental dysplasia of the hip (DDH)?
hip is in socket
however due to the shallow nature of the socket hip will pop in and out
what is dislocation in developmental dysplasia of the hip (DDH)?
packaging disorder been so severe that the hip has never been inside the socket (develops outside)
therefore socket has very shallow cup
what are the risk factors for developmental dysplasia of the hip (DDH)?
female 6:1
first born
breech
FHx
oligohydramnios (not enough fluid within the amniotic sac)
in which populations is developmental dysplasia of the hip (DDH) more common?
Native American populations and Laplanders
due to the habit of swaddling of the hip
how is developmental dysplasia of the hip (DDH) examined for?
usually picked up on newborn baby check – screening
range of motion in the hip examined
- usually limitation in hip abduction
- leg length (Galeazzi test)
3 months or older -Barlow and Ortalani tests are non-sensitive
how is developmental dysplasia of the hip (DDH) investigated?
ultrasound – birth to 4 months
after 4 months - x-ray
prior to 6 weeks -needs to be age adjusted (abnormal examinations in premature children)
measures acetabular dysplasia and the position of hip
why is an x-ray only used after 4 months of age?
no benefit prior to this
secondary ossification centres of the hip have not yet ossified
how is developmental dysplasia of the hip (DDH) usually treated?
Pavlik harness
holds leg flexed and abducted to hold femoral head within the acetabulum (concentric pressures through the hip joint for normal development)
when is a Pavlik harness used to treat developmental dysplasia of the hip (DDH)?
reducible hip
<6 months old
what treatment is used if a Pavlik harness fails/abnormality is picked up late?
MUA (manipulation under anaesthetic) + closed reduction and Spica
when is surgery used to treat developmental dysplasia of the hip (DDH)?
failed Pavlik harness
6-18 months (secondary changes to capsule + soft tissue)
what is congenital Talipes Equinovarus?
congenital deformity of the foot (“club foot”)
who is most likely to suffer from congenital Talipes Equinovarus?
1:1000
highest in Hawaiians
M2:1F
50% are bilateral
how does genetics affect congenital Talipes Equinovarus?
genetic link (PITX1 gene)
approx. 5% likely of future siblings
familial in 25%
what are the 4 aspects of a congenital Talipes Equinovarus deformity?
cavus – high arch: tight intrinsic flexor halluxes longus and flexor digitorum longus
adductus of foot: tight tibia posterior and anterior
varus: tight tendoachilles, tibia posterior and anterior
equinous: tight tendoachilles
what is the ideal method of treatment to correct congenital Talipes Equinovarus?
Ponseti Method
1 - series of casts to correct deformity
2- many require operative treatment (usually just soft tissue releases)
3 - foot orthosis brace
4 - some will require further operative intervention to correct final deformity (e.g. further soft tissue releases, significant operative interventions such as tendon transfers)
what is achondroplasia?
abnormality in the proliferation zone of the physis (inhibition of chondrocyte proliferation )
defective endochondral bone formation (secondary endochondral ossification)
what causes achondroplasia?
autosomal dominant
G380 mutation of the FGFR3
what is the usual deformity that is seen in achondroplasia?
Rhizomelic dwarfism
- humerus shorter than forearm
- femur shorter than tibia
- normal trunk
- adult height -approx. 125cm
- usually causes significant spinal issues
what is osteogenesis imperfecta?
brittle bone disease
what causes osteogenesis imperfecta?
hereditary – autosomal dominant or recessive
decreased Type I collagen due to:
- decreased secretion
- production of abnormal collagen
insufficient osteoid production
what are the orthopaedic effects of osteogenesis imperfecta?
fragility fractures
- prone to multiple fractures
short stature
scoliosis (other spinal manifestions)
what are the non-orthopaedic effects of osteogenesis imperfecta?
cardiac issues
blue sclera
dentinogenesis imperfecta – brown soft teeth
Wormian skull (abnormal fusion of cranial sutures)
hypermetabolism (typically affects parathyroid pathway)
how can fractures be described?
pattern
anatomy
intra/extra articular
displacement
what is Salter-Harris classification?
classification of physis fracture in children
what is an avulsion fracture?
bone has been pulled off by its ligamentous attachment
what are the 4 types of displacement?
displaced (ends move away from each other)
angulated (both parts at an angle to each other)
shortened (ends move towards each other)
rotated
why is primary bone healing preferred in intra articular fracture?
minimises risk of post traumatic arthritis
what is important to consider when describing a fracture in children?
both proximal and distal bone have secondary ossification centres (physis) - location
different fracture patterns (plastic deformity)
faster healing potential and remodelling potential (more allowance in displacement, shortening, angulation)
what is type 1 Salter-Harris physeal injury?
physeal separation (injury goes straight through physis)
what is type 2 Salter-Harris physeal injury (most common)?
fracture transverses through physis
exits above physis or through metaphysis
what is type 3 Salter-Harris physeal injury?
fracture traverses physis
exits epiphysis
what is type 4 Salter-Harris physeal injury?
fracture passes through epiphysis, physis, metaphysis
what is type 5 Salter-Harris physeal injury?
crush injury to physis
how does risk increase by Salter-Harris classification?
risk of growth arrest increases from 1 -5
how can the effects of physeal injury vary between younger and older children?
closer to physeal closure (older) - only small amount of potential growth left (growth arrest less concerning)
potential for growth arrest in young children is greater
what does injury to the whole physis cause in terms of growth arrest?
limb length discrepancy
what does partial injury to the physis cause in terms of growth arrest?
angulation
non affected side keeps growing
what are the aims of treatment of growth arrest?
correct deformity
minimise limb length discrepancy or angulation
what are the 2 methods of limb length correction?
shorten the long side
lengthen the short side
how does shortening the long side correct limb length?
prematurely stop growth of unaffected side to balance limb length
how can the long side be shortened in limb length correction?
prematurely fused physis of bone using crossed screws
how can the short side be lengthened in limb length correction?
intra-medullary device that is a limb lengthening device
what are the 2 methods of correcting angular deformity?
stop the growth of the unaffected side
reform the bone (osteotomy)
what must be considered in paediatric reduction of bone?
plastic deformity/increased elasticity of bone
consider soft tissue injuries and neurovascular structures that might be affected by energy dissipation during fracture
why are closed reduction techniques (traction, manipulation in A&E) more common in children?
greater remodelling potential
what is the principle behind gallows traction?
skin traction applied to femur with a weight
hold the long bones of the lower limb whilst the fracture heals
what is an issue with healing in younger children?
overgrowth, too much healing
what are the external methods of restricting a fracture?
e.g. splints, plaster
what are the internal methods of restricting a fracture?
e.g. plate and screws, intramedullary nail
what methods of restriction are more common in paediatric orthopaedics?
external (more remodelling capacity - operations can be avoided)
what is a Spica cast?
used in very young children
holds lower limbs in place
when are operative interventions more likely to be required in paediatric orthopaedics?
fracture affects the physis
correct potential deformity
(metalwork will likely need to be removed later due to growth)
what is the principle of using flexible titanium nails to treat fractures?
slightly elastic, help tension through intraosseous membrane to hold reduction in place
allow primary bone healing
what are 4 differentials for a limp in children?
septic arthritis
transient synovitis
perthes
SUFE
what is septic arthritis?
bacterial infection in intra articular space of the joint
can cause irreversible long term damage to a joint
how does septic arthritis cause irreversible long term damage to a joint?
necrosing effect of proteases that are created within the joint itself
pressure effect from chondrocytes and cartilage due to oedema within closed space
how is septic arthritis managed?
surgical wash out (lavage) of the joint to clear the infection
antibiotics
(immobilise joint in acute phase, physiotherapy if necessary)
why is septic arthritis so problematic?
sometimes challenging and difficult to diagnose
how is probability of septic arthritis classified?
Kocher’s classification
what aspects of a history are important in diagnosis of septic arthritis?
duration (chronic vs acute?)
other recent illness
associated joint pain
any other symptoms e.g. rashes, vomiting, diarrhoea
what is a typical septic arthritis history?
child previously fit and well
gone off food and drink over the last 24-48 hours
does not want to move knee and hip
what are the 4 criteria in Kocher’s classification for septic arthritis?
non weight bearing
ESR > 40
WBC > 12,000
temperature > 38
(more categories = increased likelihood)
what is a key differential for septic arthritis (or a diagnosis once septic arthritis is excluded)?
transient synovitis
what is transient synovitis?
inflamed joint in response to a systemic illness (usually coryzal)
how is transient synovitis treated?
supportive measures e.g. fluids, observation and antibiotics
what is Perthes disease?
idiopathic necrosis of proximal femoral epiphysis
in which populations is Perthes disease more likely?
usually in those 4-8 years old
male 4:1 female
what are the key differences between Perthes disease and septic arthritis?
Perthes more chronic than septic arthritis (and transient synovitis)
no temperature or inflammatory markers
(must exclude septic arthritis first)
what is the key diagnostic test for Perthes disease?
plain film radiograph
epiphysis is not as symmetrical and well-formed as the other side
how is Perthes disease managed/treated?
supportive
referral for continued observation and management
what is SUFE (slipped upper femoral epiphysis)?
proximal epiphysis slips in relation to the metaphysis
in which populations is SUFE (slipped upper femoral epiphysis) more likely?
usually obese adolescent male
12-13 years old during rapid growth
what are risk factors for SUFE (slipped upper femoral epiphysis)?
FHx
underlying endocrine disorder (hypothyroidism, hypopituitarism)
how is SUFE (slipped upper femoral epiphysis) differentiated from septic arthritis?
no temperature or raised biochemical markers
how can the presentation of SUFE be broadly differentiated?
chronic vs acute
(can be both -episodes of pain and limping in the past, now worsened)
classification to assess weight bearing
what is non-specific low back pain?
pain not due to anyspecificor underlying disease that can be found
(investigations must be done to try and find underlying cause)
what is mechanical low back pain?
painafter abnormal stress and strain on the vertebral column
what is sciatica/nerve root pain?
painradiating to the lower limbs with or without neuralgic symptoms
what kind of pain is associated with sciatica/nerve root pain?
burning, aching
maybe associated pins and needles
sometimes sensory loss
what are the main mechanical causes of lower back pain? (accounts for most low back pain cases)
disc degeneration
disc herniation
annular tears
facet joint osteoarthritis
instability
how can disc herniation cause lower back pain?
disc has slipped from vertebral body
may compress a nerve and cause nerve symptoms
what are annular tears?
rips within the disc that allow inner material (nucleus pulposus) to leak out
how can annular tears cause lower back pain?
nucleus pulposus leakage into outer margins of disk
irritation due to prostaglandins, interleukins, tumour necrosis factor etc.
how can facet joint osteoarthritis cause lower back pain?
cartilage breakdown between facet joints
lack of cartilage causes pain, loss of motion, stiffness
what are the facet joints?
2 joints at the back of the vertebrae that join vertebrae at each level
how can instability cause lower back pain?
intense wear and tear causes bones to move out of position (causes pain in itself)
damage to surrounding tissue
what are some non-mechanical causes of low back pain?
tumour - multiple myeloma (important to treat)
infection (e.g. tuberculosis of the spine)
spondyloarthropathy
pars interarticularis injury
compression fracture
visceral
what is spondyloarthropathy?
inflammatory joint disease (e.g. ankylosing spondylitis, psoriatic arthritis - usually rheumatological intervention)
what kind of people are likely to suffer from spondyloarthropathy?
middle age to younger years
why is it important to treat spondyloarthropathic conditions quickly?
causes disability
what is the pars interarticularis?
part of the vertebra between inferior and superior articular processes of the facet joint
what causes pars interarticularis injuries?
stress fractures usually occurring in adolescence due to strenuous activities such as dance, gymnastics etc.
why is it important to catch pars interarticularis injuries quickly?
stopping strenuous activity allows spontaneous healing
otherwise fractures worsen, instability occurs
what can cause compression fractures?
if osteoporotic, everyday activities
otherwise, trauma radiating through spinal column (e.g. jumping off a building and landing on feet)
how can visceral pain cause low back pain?
referred pain from another area
e.g. aortic dissection, pancreatitis etc.
what are indicators of sciatica?
unilateral leg pain greater than low back pain
pain radiating to foot or toes (may just be to knees depending on nerve affected)
numbness and paraesthesia in the same distribution (variable - depends if sensory nerves are affected)
straight leg raising test induces more leg pain (moves nerves - if trapped, causes pain)
localised neurology i.e. symptoms limited to one nerve root (combine with history and imaging)
what are the NICE guidelines for imaging in low back pain?
do not routinely offer imaging in a non-specialist setting for people with low back pain with or without sciatica
explain to people with low back pain with or without sciatica that if they are being referred for specialist opinion, they may not need imaging
consider imaging in specialist settings of care (for example, a musculoskeletal interface clinic or hospital) for people with low back pain with or without sciatica only if the result is likely to change management
what are some treatments for low back pain (according to NICE guidelines)?
injections
exercise
corsets
traction
manipulation
acupuncture
ultrasound therapy
transcutaneous nerve stimulation
psychological therapy
NSAIDS
paracetamol
weak opioids
opioids
radiofrequency denervation
epidural
spinal fusion
disc replacement
how can low back pain be treated conservatively?
analgesia (paracetamol) - (morphine rarely effective, risk of addiction)
anti-inflammatory drugs (ibuprofen)
manipulation to attempt realignment etc. (chiropractors, osteopaths, physiotherapists)
acupuncture
massage to loosen muscle spasm
allow some time to pass - most heal spontaneously
why does bed rest not result in faster recovery for low back pain?
muscle atrophy makes movement more difficult
what are the red flag symptoms for low back pain?
weight loss
fever
night pain
under 19 years
what may weight loss indicate as a red flag symptom for low back pain?
cancer
infection
what may night pain indicate as a red flag symptom for low back pain?
malignancy involving bones
may just be from turning over etc.
what is the problem with the red flag symptoms for low back pain?
insufficient evidence (e.g. no research suggesting weight loss percentage association with serious disease)
what are the symptoms of cauda equina syndrome/red flag symptoms for leg pain?
bladder or bowel dysfunction
saddle anaesthesia
neurological deficit in legs
what should be done if cauda equina syndrome is suspected?
imaging and treatment immediately
what are 2 common metastatic malignancies that are involved with low back pain?
breast cancer
prostate cancer
why is it important not to wait too long when dealing with malignancies associated with low back pain?
risk of weak bones collapsing
may cause severe fracture, compression of the spinal cord and paralysis
why is it important not to wait too long when dealing with inflammatory arthropathy associated with low back pain?
early diagnosis for effective treatment with biologics
what does a malignancy (low back pain) look like on an MRI?
areas of disease show up white within spinal column (water oedematous)
CSF shows up as white
what does a inflammatory arthropathy (low back pain) look like on an MRI?
shiny corner on vertebra
oedema due to inflammatory process
what MRI scans are done when checking for inflammatory arthropathy (low back pain) ?
whole spine
sacrum
leg joints
why is it important not to wait too long when dealing with myeloma associated with low back pain?
early diagnosis catches disease at more treatable stage
why is it important not to wait too long when dealing with tuberculosis associated with low back pain?
early diagnosis catches disease at more treatable stage
prevents spinal collapse, compression, paralysis
what are primary investigations in imaging for low back pain?
MRI
what are primary investigations in imaging for low back pain?
radiographs, CT
why is an MRI the most effective investigation for low back pain imaging?
shows destruction, oedema and swelling in bone marrow
what are the benefits of x-rays?
cheap
readily available
traditional
what are the disadvantages of x-rays compared to MRIs?
radiation (moderate, not high risk)
overlook details of many important diseases (e.g. sarcoma related to Paget’s disease)
what are the disadvantages of radiographs compared to MRIs?
miss lesions
what is an osteoid osteoma?
benign tumour of bone
displaces bone around
how does an osteoid osteoma present on a CT?
small hole
large area of white (lateral view may look like inflammatory arthropathy)
how is an osteoid osteoma treated?
ablation
needle inserted using CT control, heated
what are the clinical signs of a fracture?
pain
swelling
crepitus
deformity
adjacent structural injury (nerves, vessels, tendons, ligaments)
what are some general fracture complications?
fat embolus (hours)
deep vein thrombosis (days-weeks)
pulmonary embolism
infection/sepsis
prolonged immobility (UTI, chest infections, sores)
what are some urgent local complications of fractures?
local visceral injury
vascular injury
nerve injury
compartment syndrome
haemarthrosis
infection
gas gangrene
what is compartment syndrome?
pressure within a compartment increases, restricting blood flow and damaging structures
what are some less urgent local complications of fractures?
fracture blisters
plaster sores
pressure sores
nerve entrapment
myositis ossificans
ligament injury
tendon lesions
joint stiffness
algodystrophy
what are the 3 types of joint classified by structure?
fibrous
cartilaginous
synovial
what are the 3 types of fibrous joint?
sutures
syndesmosis
interosseous membrane
what are the 2 types of cartilaginous joint?
synchondroses (e.g. spine)
symphyses (e.g. pubic)
what are the 6 types of synovial joint?
plane (e.g. between tarsal bones)
hinge (e.g. elbow)
condyloid (e.g. between radius and carpal bones in wrist)
pivot (e.g. between C1 and C2 vertebrae)
saddle (e.g. between trapezium carpal bone and first metacarpal bone)
ball and socket (e.g. hip)
how are synovial joints stabilised?
muscles/tendons
ligaments
bone surface congruity
what is the structure of a synovial joint?
joint cavity filled with synovial fluid between bone
lined with articular cartilage
what is the structure of the synovium?
1-3 cell deep lining
contains type A synoviocyte - macrophage-like phagocytic cells
contains type B synoviocyte - fibroblast-like cells that produce hyaluronic acid
type I collagen
what is synovial fluid?
hyaluronic acid-rich viscous fluid
what is the structure of articular cartilage?
type II collagen
proteoglycan (aggrecan)
what 2 things is cartilage composed of?
specialized cells (chondrocytes)
extracellular matrix - water, collagen and proteoglycans
mainly aggrecan
what is aggrecan?
proteoglycan
possesses many chondroitin sulfate and keratin sulfate chains
what is aggrecan characterised by?
ability to interact with hyaluronan to form large proteoglycan aggregates
what are the 2 major divisions of arthritis?
osteoarthritis
inflammatory arthritis (main type - rheumatoid arthritis)
how do radiographic changes differ in rheumatoid arthritis and osteoarthritis?
joint space narrowing - both
subchondral sclerosis - rheumatoid arthritis
osteophytes - osteoarthritis
osteopenia - rheumatoid arthritis
bony erosion - rheumatoid arthritis
what is the pathophysiology of osteoarthritis?
degradation of chondral cartilage
inflammation occurs late compared to rheumatoid arthritis
inflammatory mediators include proteinases, inflammatory cytokines (enhance synthesis of proteinases and other catabolic factors to degrade articular cartilage membrane)
what are the main risk factors for osteoarthritis?
age
excess weight
mechanical constraints (e.g. extreme sports)
heredity
female gender, menopause
osteonecrosis
leg bone malalignment
oestrogen deficiency
metabolic syndorme
advanced hip osteoarthritis (spondyarthritis or rheumatoid)
what are the non-major risk factors for osteoarthritis?
injury (cruciate ligament rupture, menisectomy)
metabolic disease (chondrocalcinosis, genetic haemochromatosis)
infectious diseases involving bone
rheumatoid arthritis sequellae
what should be assessed in osteoarthritis?
pain (exertional/rest/night)
disability (walking distance/stairs/giving way)
deformity
previous history (trauma/infection)
treatments given (physio/injections/operations)
other joints affected
how is osteoarthritis assessed?
look
feel
move
special tests
what are some signs of ACL injury?
valgus alignment, walk with antalgic gait
small effusion on palpation
knee flexion is 70 degrees compared with healthy knee
positive anterior drawer consistent with ACL
what are the 4 radiographic changes of osteoarthritis?
osteophyte
loss of joint space
subchondral cysts
sclerosis
what are some conservative methods of osteoarthritis management?
analgesics
physiotherapy
walking aids
avoidance of exacerbating activity
injections (steroid/viscosupplementation)
what are some operative methods of osteoarthritis management?
replace (knee/hip)
realign (knee/big toe)
excise (toe)
fuse (big toe)
synovectomy (rheumatoid)
denervate (wrist)
what are the risk factors for septic arthritis?
immunosuppressed
pre-existing joint damage
intravenous drug use
how is septic arthritis diagnosed?
joint aspiration
gram stain and culture of sample
how is osteomyelitis treated?
IV antibiotics
surgical drainage, especially collections/sequestrum
chronic - antibiotic suppression/dressings
(amputation)
what are the most common shoulder conditions in 15-45 year olds?
dislocation
fractures
what are the most common shoulder conditions in 45-60 year olds?
dislocation
fractures
impingement
acromioclavicular joint osteoarthritis
rotator cuff tears
what are the most common shoulder conditions in 60+ year olds?
fractures
impingement
rotator cuff tears
glenohumeral osteoarthritis
what are the most common hip conditions in 15-45 year olds?
developmental dysplasia
leg length discrepancy
impingement
what are the most common hip conditions in 45-60 year olds?
impingement
osteoarthritis
avascular necrosis
what are the most common hip conditions in 60+ year olds?
osteoarthritis
post total hip replacement
what are the most common knee conditions in 15-45 year olds?
patellofemoral maltracking
ACL/PCL
meniscal tears
fractures
what are the most common knee conditions in 45-60 year olds?
osteoarthritis
patellofemoral maltracking
ACL/PCL
meniscal tears
fractures
what are the most common knee conditions in 60+ year olds?
osteoarthritis
what radiology investigations are done for bone or joint infection?
plain films
MRI scans: bony architecture/collections (CT if MRI not available)
bone scans: multifocal disease
labelled white cell scans
what blood tests are done for bone or joint infection?
CRP: acute marker
ESR (slower response)
WCC
TB culture/PCR
how can stress cause a fracture?
overuse - stress exerted overcomes remodelling capacity
bone weakens, causes stress fracture
what are the weight bearing bones?
femur
tibia
metatarsals
navicular
what some activity related stressors that can cause fractures?
athletes
military
female athletes (female athlete triad)
what are 3 factors contributing to secondary osteoporosis?
hypogonadism
glucocorticoid excess
alcoholism
what is Paget’s disease?
excessive bone break down and disorganized remodelling
causes deformity, pain, fracture or arthritis
may become malignant
what are the 4 stages of Paget’s disease?
osteoclastic Activity
mixed osteoclastic-osteoblastic activity
osteoblastic activity
malignant degeneration
what are the 4 primary bone cancers?
osteosarcoma
chondrosarcoma
Ewing sarcoma
lymphoma
what are the 4 malignancies that cause lytic bone damage?
kidney
thyroid
lung
breast
what are the 2 malignancies that cause blastic bone damage?
prostate
breast
what are the 3 forms of tendinopathy?
tendinosis (abnormal thickening)
tendinitis (inflammation)
rupture
how are ligament injuries classified?
grade 1 to 3
what are the features of a grade 1 ligament injury?
slight incomplete tear, stretching
no notable joint instability
what are the features of a grade 2 ligament injury?
moderate/severe incomplete tear
some joint instability.
1 ligament may be completely torn
what are the features of a grade 3 ligament injury?
complete tearing of 1 or more ligaments
obvious instability
surgery usually required
how can tendon or ligament tears be managed conservatively?
immobilise (plaster, boot or brace)
how can tendon or ligament tears be managed surgically/operatively?
suture
what are the benefits of immobilisation on injured ligamentous tissue?
less ligament laxity
what are the benefits of mobilisation on injured ligamentous tissue?
ligament scars are wider, stronger, more elastic
better alignment/quality of collagen
what are the disadvantages of immobilisation on injured ligamentous tissue?
less overall strength of ligament repair scar
protein degradation exceeds protein synthesis (decreased collagen quantity)
production of inferior tissue by blast cells
resorption of bone at site of ligament insertion
decreased tissue tensile strength
how do ligaments heal?
inflammatory phase - tissue damage
proliferative phase - growth factors/cytokines
tissue remodelling -collagenase, enzymes, macrophages to form structure
what is the purpose of the inflammatory phase in ligamentous healing?
debris clearance
what cells are involved in the inflammatory phase in ligamentous healing?
platelets, macrophages activate mast cells, neutrophils and phagocytes
what is the purpose of the proliferative phase in ligamentous healing?
new collagen
angiogenesis
neovascularisation
what cells are involved in the proliferative phase in ligamentous healing?
fibroblasts
endothelial cells
myofibroblasts
how can the healing environment be divided?
mechanical environment
biological environment
what 2 things make up the mechanical environment for healing?
movement
forces
what 4 things make up the mechanical environment for healing?
blood supply
immune function
infection
nutrition
what are the 2 components of bone matrix?
organic
inorganic
what 2 things make up the organic component of bone?
type 1 collagen (90%)
ground substance
what 2 things make up the inorganic component of bone?
calcium hydroxyapatite
osteocalcium phosphate
what 3 things make up the ground substance in the organic component of bone?
proteoglycans
glycoproteins
cytokines and growth factors
what is appositional growth?
deposition of bone beneath the periosteum to increase thickness
what are the 4 stages of appositional growth?
ridges in periosteum create groove for periosteal blood vessel
periosteal ridges fuse, forming endosteum-lined tunnel
osteoblasts in endosteum build new concentric lamellae inward toward centre of tunnel, forming new osteon
bone grows outwards as osteoblasts in periosteum build new circumferential lamellae
(osteon formation repeats as new periosteal ridges fold over blood vessel)
what are the 3 types of joint classified by function?
synarthosis (no movement allowed)
amphiarthroses (limited movement allowed)
diarthroses (free movement - synovial only)
what signs and symptoms is osteoarthritis associated with?
joint pain (worse with activity)
joint crepitus
joint instability (‘giving way’)
joint enlargement
e.g. Heberden’s nodes
joint stiffness after immobility (‘gelling’)
limitation of range of motion
how does inflammation manifest clinically?
rubor (redness)
dolor (pain)
calor (heat)
tumor (swelling)
loss of function
what are the 3 causes of joint inflammation?
infection (e.g. septic arthritis, tuberculosis)
crystal arthritis (e.g. gout, pseudogout)
immune-mediated (“autoimmune”) (e.g. rheumatoid, psoriatic, reactive arthritis, systemic lupus erythematosus (SLE))
what is gout?
form of crystal arthritis
syndrome caused by deposition of monosodium urate (uric acid) crystals leading to inflammation
causes gouty arthritis, tophi
what is the main risk factor for gout?
hyperuricaemia
what are 3 causes of hyperuricaemia?
genetic tendency
increased intake of purine rich foods
reduced excretion (kidney failure)
what is pseudogout?
form of crystal arthritis
syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) leading to inflammation
what are the main risk factors for psuedogout?
background osteoarthritis
elderly patients
intercurrent infection
where does gout usually present?
first metatarsophalangeal joint most common (podagra)
foot, ankle, knee, wrist, finger, and elbow joints most frequently affected
how is crystal arthritis diagnosed?
aspirating fluid from affected joint - synovial fluid analysis
examining it under a microscope using polarized light
gram stain - culture, antibiotic sensitivity assays
how can gout be diagnosed from a synovial fluid analysis?
needle shaped crystals
negative birefringence
how can pseudogout be diagnosed from a synovial fluid analysis?
rhomboid/brick shaped crystals
positive birefringence
what are the 3 key features of rheumatoid arthritis?
chronic arthritis
extra articular disease (rheumatoid nodules, rarely vasculitis, episcleritis)
rheumatoid factor may be detected in blood
how can the pattern of joint involvement in rheumatoid arthritis be described?
symmetrical
affects multiple joints (polyarthritis)
affects small and large joints, but particularly hands and feet
what is the primary site of pathology in rheumatoid arthritis?
synovium
includes
- synovial joints
- tenosynovium surrounding tendons
- bursa
what are the common extra articular features in rheumatoid arthritis?
fever
weight loss
subcutaneous nodules
what are the uncommon extra articular features in rheumatoid arthritis?
vasculitis
ocular inflammation (e.g. episcleritis)
neuropathies
amyloidosis
lung disease – nodules, fibrosis, pleuritis
Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis
what are subcutaneous nodules in rheumatoid arthritis?
central area of fibrinoid necrosis
surrounded by histiocytes and peripheral layer of connective tissue
the synovial membrane is abnormal in rheumatoid arthritis - why does the synovium become a proliferated mass of tissue?
neovascularisation
lymphangiogenesis
inflammatory cells:
- activated B and T cells
- plasma cells
- mast cells
- activated macrophages
excess of pro-inflammatory cytokines promotes excessive recruitment, activation and effector functions
what is is the dominant pro-inflammatory cytokine in the rheumatoid synovium for the pathogenesis of rheumatoid arthritis?
tumour necrosis factor alpha (TNFα)
how can tumour necrosis factor alpha (TNFα) be inhibited in treatment of rheumatoid arthritis?
antibodies or fusion proteins
parenteral administration (most commonly subcutaneous injection)
what are the 2 types of autoantibody generally found in rheumatoid arthritis patients?
rheumatoid factor
antibodies to citrullinated protein antigens (e.g. anti-cyclic citrullinated peptide antibody or ‘anti-CCP antibody’)- highly specific for rheumatoid arthritis, associated with worse prognosis
what is rheumatoid factor?
anti-IgG (Fc portion) and IgM
i.e. IgM anti-IgG antibody
what does effective management of rheumatoid arthritis require?
early recognition of symptoms, referral and diagnosis
prompt initiation of treatment: joint destruction = inflammation x time
aggressive treatment to suppress inflammation
what drugs are used to treat rheumatoid arthritis?
disease modifying anti-rheumatic drugs (DMARD) to control disease process
1st line treatment:
methotrexate with hydroxychloroquine or sulfasalazine
how are biological therapies used to treat rheumatoid arthritis (2nd line)?
proteins (usually antibodies) that specifically target a protein such as an inflammatory cytokine
what are 4 biological therapies used to treat rheumatoid arthritis (2nd line)?
inhibition of tumour necrosis factor-alpha (‘anti-TNF’)
- antibodies
- fusion proteins
B cell depletion
– antibody against B cell antigens
modulation of T cell co-stimulation
inhibition of interleukin-6 signalling
– antibody against interleukin-6 receptor
what is psoriatic arthritis?
psoriasis - autoimmune disease affecting the skin (scaly red plaques on extensor surfaces)
some patients also have joint inflammation
how does psoriatic arthritis present?
classically asymmetrical arthritis affecting interphalangeal joints
can also manifest as:
- symmetrical involvement of small joints (rheumatoid pattern)
- spinal and sacroiliac joint inflammation
- oligoarthritis of large joints
- arthritis mutilans
what is reactive arthritis?
sterile inflammation in joints following infection
especially urogenital and gastrointestinal infections (may be mild)
may be first manifestation of HIV or Hep C infection
what are 3 important extra articular manifestations of reactive arthritis?
skin inflammation
eye inflammation
enthesitis (tendon inflammation)
who is most likely to suffer from reactive arthritis?
commonly young adults with genetic predisposition (e.g. HLA-B27) and environmental trigger (i.e. infection
symptoms follow 1-4 weeks after infection
what are the key differences between septic and reactive arthritis?
synovial fluid culture - positive in septic, sterile in reactive
antibiotic therapy and joint lavage (in large joints) for septic arthritis
what are tophi?
aggregated deposits of monosodium urate (uric acid) crystals in tissue
how does gout present?
abrupt onset
extremely painful
joint red, warm, swollen and tender
resolves spontaneously over 3-10 days
how can gout be seen on an x-ray?
juxta-articular ‘rat bite’ erosions
how is an acute attack of gout managed?
colchicine
NSAIDs
steroids
how is chronic gout managed?
allopurinol (lowers levels of uric acid)
what is ankylosing spondylitis?
seronegative spondyloarthropathy (no positive autoantibodies)
chronic sacroiliitis (inflammation of sacroiliac joints)
results in spinal fusion – ankylosis
what demographic is most likely to suffer from ankylosing spondylitis?
20-30 year old
male
(back pain > 3 month in < 45 year olds - suggestive)
what gene is ankylosing spondylitis associated with?
HLA B27
how does ankylosing spondylitis present clinically?
lower back pain + stiffness (early morning, improves with exercise)
reduced spinal movements
peripheral arthritis
plantar fasciitis, Achilles tendonitis
fatigue
altered posture - hyperextended neck, loss of lumbar lordosis, flexed hips and knees
what blood test results are seen in ankylosing spondylitis?
normocytic anaemia
raised CRP, ESR
HLA-B27
what imaging results are seen in ankylosing spondylitis?
x-ray
MRI
- squaring vertebral bodies, Romanus lesion
- erosion, sclerosis, narrowing sacroiliac joint
- bamboo spine
- bone marrow oedema
how is ankylosing spondylitis managed?
physiotherapy
exercise regimes
NSAIDs
peripheral joint disease - DMARDs
what investigations are done for psoriatic arthritis?
x-rays of affected joints – pencil in cup abnormality
MRI – sacroiliitis and enthesitis
bloods – no antibodies as seronegative
how is psoriatic arthritis managed?
DMARDs – methotrexate
why are oral steroids avoided in management of psoriatic arthritis?
risk of pustular psoriasis due to skin lesions
what is systemic lupus erythematous (SLE)?
multi-system autoimmune disease
multi-site inflammation (often joints, skin, kidneys, haematology - involves lungs and CNS)
autoantibodies for components of cell nucleus (nucleic acids and proteins)
how can autoantibodies be used diagnostically in systemic lupus erythematous (SLE)?
antinuclear antibodies (ANA):
- high sensitivity for SLE but not specific
- negative test rules out SLE, but a positive test does not mean SLE
anti-double stranded DNA antibodies (anti-dsDNA Abs):
- high specificity for SLE in the context of the appropriate clinical signs
(anti-phospholipid antibodies)
which demographic is systemic lupus erythematous (SLE) most common in?
9F:1M
15 - 40 yrs
increased prevalence in African and Asian ancestry populations
what are the 3 types of diagnostic test done in rheumatology?
blood test
synovial fluid analysis
imaging
- x-ray
- ultrasound
- CT
- MRI
what are the basic rheumatology blood tests?
full blood count (FBC)
urea and electrolytes (U&E) - urea, sodium, potassium, creatinine
liver function tests (LFT) - bilirubin, ALT, ALP, albumin
bone profile - ALP, calcium, phosphate
erythrocyte sedimentation rate (ESR)
C-reactive protein (CRP)
how do haemoglobin levels vary between inflammatory arthritis, osteoarthritis and septic arthritis (in FBC)?
inflammatory arthritis - low Hb (anaemia) or normal
osteoarthritis - normal
septic arthritis - usually normal
how does MCV vary between inflammatory arthritis, osteoarthritis and septic arthritis (in FBC)?
inflammatory arthritis - normal
osteoarthritis - normal
septic arthritis - normal
how does WCC vary between inflammatory arthritis, osteoarthritis and septic arthritis (in FBC)?
inflammatory arthritis - usually normal
osteoarthritis - normal
septic arthritis - raised WCC (leucocytosis)
how does PLT (platelet count) vary between inflammatory arthritis, osteoarthritis and septic arthritis (in FBC)?
inflammatory arthritis - normal or raised
osteoarthritis - normal
septic arthritis - normal or raised
what does a high creatinine indicate as part of rheumatological diagnostics?
worse renal clearance (indicating kidney problem)
what are some examples of rheumatological diseases affecting the kidneys?
systemic lupus erythematous (SLE) causes lupus nephritis
vasculitis leads to nephritis
chronic inflammation in poorly controlled inflammatory disease leads to high levels of serum amyloid A protein, deposits in organs (AA amyloidosis)
(NSAIDs used in treatment may cause kidney impairment)
why are LFTs important in rheumatological diagnostics?
DMARDs can cause liver damage - patients need regular tests
what can low albumin as a result in LFTs indicate? (rheumatological diagnostics)
problem of synthesis (in liver)
problem of leak from kidney (e.g. in lupus nephritis)
what are the results of a bone profile in Paget’s disease?
raised ALP
what are the results of a bone profile in osteomalacia?
ALP - normal or raised
Ca and PO4 - normal or low
what are the results of a bone profile in osteoporosis?
ALP, PO4, Ca - usually normal
what are some other (non-inflammatory) reasons for raised ESR?
elevated immunoglobulin level
paraprotein (myeloma)
anaemia
tends to rise with age
how are ESR and CRP used in diagnosis of systemic lupus erythematosus (SLE)?
usually - ESR high, CRP normal
(CRP high if synovitis or inflammatory pleural/pericardial effusion)
should have low index of suspicion for infection if CRP raised
what are some non-specific causes for the presence of anti-nuclear antibodies (ANA)?
relatively common in general healthy population at low titre (level)
prevalence generally increases with age
sometimes transiently positive following infection
what may a high titre of anti-nuclear antibodies (ANA) indicate?
autoimmune connective tissue disease (SLE, scleroderma, Sjogren’s syndrome)
stronger test is more likely to be clinically significant
must be in combination with correct clinical features
how is an ANA (anti-nuclear antibody) test interpreted?
strength reported as maximal dilution at which it is still detectable
e.g. 1:80 (weak), 1:320, 1:640, 1:1280 (strong)
negative test rules out SLE
positive test does not necessarily mean SLE, but suggestive IF there are other clinical and lab features to support the diagnosis
what other tests are ordered if an ANA test is positive?
ENA (extractable nuclear antigens):
- Ro - lupus or Sjogren’s syndrome
- La - lupus or Sjogren’s syndrome
- RNP - lupus or mixed connective tissue disease
- Smith - lupus
- Jo-1 - polymyositis
complement C3 and C4 - may be low in active lupus
dsDNA (double stranded DNA) antibodies - highly specific for lupus, associated with renal involvement, useful for tracking lupus activity over time
what are the benefits of x-rays in rheumatology?
first line
cheap
widely available
what are the benefits of CT scans in rheumatology?
more detailed bony imaging
what are the benefits of MRIs in rheumatology?
best visualization of soft tissue structures like tendons and ligaments
best for spinal imaging: can see spinal cord and exiting nerve roots
what are the disadvantages of MRIs in rheumatology?
expensive
time-consuming
what are the benefits of an ultrasound in rheumatology?
visualise soft tissue structures
what are the disadvantages of ultrasounds in rheumatology?
good for smaller joints - less good for deep/large joints (knee or hip)
what are the radiographic features of rheumatoid arthritis?
soft tissue swelling
peri-articular osteopenia
bony erosions (only in established disease, aim to treat before this)
what are the ultrasound features of rheumatoid arthritis?
(better for detecting synovitis)
synovial hypertrophy (thickening)
increased blood flow (seen as doppler signal)
may detect erosions not seen on plain X-ray
what are the main connective tissue diseases?
systemic Lupus Erythematosus (SLE)
Sjögren’s syndrome
autoimmune inflammatory muscle disease
systemic sclerosis (scleroderma)
overlap syndromes
what are the 2 types of autoimmune inflammatory muscle disease?
polymyositis
dermatomyositis
what are the 2 types of systemic sclerosis (scleroderma)?
diffuse cutaneous
limited cutaneous
what are the seronegative spondyloarthropathies?
ankylosing spondylitis
reactive arthritis (Reiters syndrome)
psoriatic arthritis
enteropathic synovitis (arthritis associated with GI inflammation)
what phenomenon is common in connective tissue disorders?
Raynaud’s phenomenon
what is Raynaud’s phenomenon?
intermittent vasospasm of digits on exposure to cold
typical colour changes – white to blue to red
- vasospasm leads to blanching of digit
- cyanosis as static venous blood deoxygenates
- reactive hyperaemia
(usually isolated and benign)
what is the significance of serum autoantibodies in connective tissue disorders?
may aid diagnosis
correlate with disease activity
may be directly pathogenic
what are the typical clinical manifestations of systemic lupus erythematosus (SLE)?
malar rash (erythema that spares the nasolabial fold)
photosensitive rash
mouth ulcers
hair loss
Raynaud’s phenomenon
arthralgia and sometimes arthritis (non-erosive)
serositis (pericarditis, pleuritis, less commonly peritonitis)
renal disease – glomerulonephritis (‘lupus nephritis’)
cerebral disease – ‘cerebral lupus’ e.g. psychosis
what is the pathogenesis of systemic lupus erythematosus (SLE)?
apoptosis leads to translocation of nuclear antigens to membrane surface
impaired clearance of apoptotic cells results in enhanced presentation of nuclear antigens to immune cells
B cell autoimmunity
tissue damage by antibody effector mechanisms (e.g. complement activation and Fc receptor engagement)
what are anti-phospholipid antibodies associated with in systemic lupus erythematosus (SLE)?
risk of arterial and venous thrombosis
may also occur in absence of SLE in what is termed the ‘primary anti-phospholipid antibody syndrome
what autoantibodies are associated with systemic vasculitis?
antinuclear cytoplasmic antibodies (ANCA)
if an ANA test is positive, what other antibodies are screended for?
anti-Ro
anti-La
anti-centromere
anti-Sm
anti-RNP
anti-ds-DNA antibodies
anti-Scl-70
cytoplasmic antibodies
- anti-tRNA synthetase antibodies
- anti-ribosomal P antibodies
what is the significance of anti-Sm antibodies in systemic lupus erythematosus (SLE)?
specific for SLE
serum level of antibody does NOT correlate with disease activity
what is the significance of anti-Ro and anti-La antibodies in systemic lupus erythematosus (SLE)?
secondary Sjögren’s syndrome
neonatal lupus syndrome (transient rash in neonate, permanent heart block)
what is the significance of anti-ribosomal P antibodies in systemic lupus erythematosus (SLE)?
cerebral lupus
what autoantibodies are associated with diffuse systemic sclerosis?
anti-Scl-70 antibody
what autoantibodies are associated with limited systemic sclerosis?
anti-centromere antibodies
what autoantibodies are associated with dermatomyositis/polymyositis?
anti-tRNA transferase antibodies
e.g. histidyl transferase, also termed anti-Jo-1 antibodies
what autoantibodies are associated with Sjögren’s syndrome?
no unique antibodies but typically see:
- anti-Ro and anti-La antibodies
- rheumatoid factor
what autoantibodies are associated with mixed connective tissue disease?
anti-U1-RNP antibodies
how can disease activity be assessed in systemic lupus erythematosus (SLE)?
low complement C3 and C4
high anti-dsDNA antibodies
low platelet (PLT)
how is systemic lupus erythematosus (SLE) managed?
treatment aims at remission or low activity and prevention of flares
hydroxychloroquine is recommended in all lupus patients
maintenance treatment glucocorticoids minimised or withdrawn if possible
(appropriate initiation of immunomodulatory agents (methotrexate, azathioprine, mycophenolate) can expedite the tapering/discontinuation of glucocorticoids)
cyclophosphamide and B cell targeted therapies (rituximab and belimumab) for persistently active or severe disease
assess antiphospholipid antibody status, infectious and CVD risk profile
pregnancy planning
what is Sjögren’s syndrome?
autoimmune exocrinopathy
mainly lymphocytic infiltration of exocrine glands, sometimes of other organs (extra-glandular involvement)
(‘secondary’ Sjögren’s syndrome if in context of another connective tissue disorder e.g. SLE)
what does the exocrine gland pathology of Sjögren’s syndrome result in?
dry eyes (xerophthalmia)
dry mouth (xerostomia)
parotid gland enlargement
what are the most common extra-glandular manifestations of Sjögren’s syndrome?
non-erosive arthritis
Raynaud’s phenomenon
what tests can be done for Sjögren’s syndrome?
salivary gland biopsy
Schirmer’s test
how does a salivary gland biopsy test for Sjögren’s syndrome?
show lymphocytic infiltration
mostly CD4 helper T cells, B lymphocytes to lesser extent
how does a Schirmer’s test test for Sjögren’s syndrome?
assess tear production
filter paper placed under lower eyelid, extent of wetness measured after 5 minutes
abnormal result: <5mm
what is inflammatory muscle disease?
proximal muscle weakness due to autoimmune-mediated inflammation
with a rash - dermatomyositis
without a rash -polymyositis
what skin changes take place in dermatomyositis (inflammatory muscle disease)?
lilac-coloured (heliotrope) rash on eyelids, malar region and naso-labial folds
red or purple flat or raised lesions on knuckles (Gottron’s papules)
subcutaneous calcinosis
mechanic’s hands (fissuring and cracking of skin over finger pads)
what conditions is inflammatory muscle disease associated with?
malignancy
pulmonary fibrosis
how is inflammatory muscle disease diagnosed?
elevated creatinine phosphokinase
abnormal electromyography
abnormal muscle biopsy
polymyositis = CD8 T cells dermatomyositis = CD4 T cells in addition to B cells
what are the features of systemic sclerosis/scleroderma?
thickened skin with Raynaud’s phenomenon
dermal fibrosis, cutaneous calcinosis, telangiectasia
what are the features of diffuse systemic sclerosis?
fibrotic skin proximal to elbows or knees (excluding face and neck)
anti-topoisomerase-1 (anti-Scl-70) antibodies
pulmonary fibrosis, renal (thrombotic microangiopathy) involvement
short history of Raynaud’s phenomenon
what are the features of limited systemic sclerosis?
fibrotic skin hands, forearms, feet, neck and face
anti-centromere antibodies
pulmonary hypertension
long history of Raynaud’s phenomenon
what is overlap syndrome?
features of more than 1 connective tissue disorder are present
what is undifferentiated connective tissue disease?
incomplete features of a connective tissue disease are present
what is mixed connective tissue disease?
features of multiple connective tissue disorders
identified by presence of anti-U1-RNP antibody
