ortho eopt revision Flashcards
define open fracture
fracture or its hematoma that communicates with the external environment
classification for open fractures
gustilo anderson classification
what is gustilo I
size: wound < 1 cm minimal ST damage mild contaimination low impact risk of amputation: 5%
what is gustilo II
size: wound 1-10cm moderate ST injury, no flap or avulsion moderate contamination moderate commintion risk of amputation: 10%
what is gustilo III
size; wound > 10cm
extensive ST injury
significant contamination
high impact
IIIA:
adequate ST coverage of bone
risk of amputation: 20%
IIIB:
inadequate ST coverage
risk of amputation: 30%
IIIC:
arterial injury (regardless of wound size)
prophylactic faciotomy
risk of amputation: >40%
management of open fracture
1) primary survey (ABCDE, remove gross debris, tro open fracture, escalate to consultant)
2) check neurovascular status + apply direct pressure on bleeding wound
3) early management (analgesia according to WHO pain ladder, splint fracture)
4) AMPLE + XR + photograph wound
5) prepare for EOT (antibx = 1st gen cephalosporin cephalaxin +/- gentamycin for GIII, tetanus, nbm)
6) debridement + wound culture
7) repair vascular injuries + amputate crush injuries
8) remove comminuted fragments
9) dilute bacterial load with 10L saline
10) reduce, maintain & stabilise
11) 48h later: relook operation (repeat I&D? wound cover)
12) 4-6 weeks: bone graft
bone complications of open fractures
1) OM
2) arthritis
3) malunion
4) delayed union
5) non union: SPLINTS
6) AVN
causes of nonunion
SPLINTS
1) soft tissue interposition
2) position of reduction
3) location
4) infection
5) nutrition
6) tumor
7) severity of injury
regional complications of open fractures
1) neurovascular injury
2) ST blisters/fracture blisters (haemorrhagic/non)
3) complex regional pain syndrome
4) heterotopic ossification
5) joint stiffness
6) compartment syndrome (after wound closure)
7) surgical site infection
complications of compartment syndrome
1) rhabdomyolysis
2) volksmann ischaemic contracture
3) permanent functional impairment
systemic complications of open fracture
1) hypovolemic shock
2) fat embolisation
3) DVT/PE
4) MODS
5) ARDS
position of fragments in femoral shaft fracture of proximal 1/3 or midshaft
proximal: flexed, abducted, externally rotated (iliopsoas @ lesser trochanter, gluteus medius/minimus @ greater troch)
distal: adducted
position of fragmenst in distal 1/3 femoral shaft fracture
proximal: adducted
distal: flexed (gastroc)
management of femoral shaft fracture in infant
1-2 weeks: gallow’s traction
3-4 weeks: hip spica
management of femoral shaft fracture in child
3-4 weeks: traction
- child < 12kg : gallow’s traction
- older children: thomas’s splint + pearson knee attachment
6 weeks: hip spica
management of femoral shaft fracture in adolescent
traction + spica followed by ORIF + plate/screws (if reduction unsatisfactory)
management of femoral shaft fracture in adults
1) thomas splint at scene
2) ABCDEs of trauma
3) analgesia
4) manipulation & reduction with conscious sedation
5) hold with traction with thomas’ splint
6) intramedullary nail within 24h (ext fixation if open fracture)
7) early mobilisation
general complications of femoral shaft fracture
1) haemorrhage
2) shock
3) fat embolism
4) ARDS
5) MODS
6) DIVC
early complications of femoral shaft fracture
1) vascular injury: femoral artery
2) neurological injury: sciatic nerve
late complications of femoral shaft fractures
1) thromboembolism
2) fat embolism
3) infection
4) delayed union/non-union
5) malunion
6) joint stiffness (joint injury or ST adhesion)
types of proximal femur fractures
1) neck of femur
2) intertrochanteric
3) subtrochanteric
types of neck of femur fractures
1) subcapital
2) transcervical
3) basicervical
risk factors for proximal femur fractures
1) non modifiable
- old age
- F
- early menopause
- nulliparity
- family history or personal history of fractures
2) modifiable
- factors increasing risk of falls
- factors reducing bone strength (osteoporosis, steroids/smoking/alc, hypo/hyperthyroidism, physical immobility, pathological bone conditions, chronic liver/kidney conditions)
bruising suggestive of intra or extra capsular proximal femoral fracture?
extra capsular
classification for neck of femur fractures
garden’s classification
garden’s classification
type 1: incomplete impacted fracture
type 2: complete fracture, not displaced
type 3: complete fracture, moderately displaced (head in varus, internally rotated, abducted; distal externally rotated)
type 4: complete fracture, severely displaced
management of NOF fracture in <60
undisplaced: hip spica
displaced: m&r > internal fixation (cancellous screws)
management of NOF fracture in > 60
undisplaced
- 65: cancellous screw
- 90: hemiarthroplasty
displaced
- hemiarthroplasty
- THR
why is internal fixation contraindicated in displaced NOF fracture of old (>60)
risk of AVN + nonunion
general complications of NOF fracture
1) thromboembolism
2) pneumonia
3) bed sores
4) uti
fracture related complications of NOF fracture
1) AVN of femoral head (NOF fracture can sever both nutrient artery + retinacular artery, leaving ligamentum teres vessels insufficient)
2) nonunion (SPLINTS)
- <50: bone graft across fracture
- >50: hemiarthroplasty or THR
3) secondary OA
management for intertrochanteric or subtrochanteric fractures
m&r under anaesthesia + internal fixation with PFNA
causes of hip dislocation
1) septic arthritis
2) muscle imbalance
3) trauma
4) post THR (THR unstable in flexion, adduction, internal rotation)
mechanism of injury of posterior hip dislocation
dash board injury
associated injuries with posterior hip dislocation
1) PCL injury
2) posterior wall of acetabulum
3) femoral fracture
4) sciatic nerve injury
signs of posterior hip dislocation
1) shortened limb
2) hip adducted, internally rotated and flexed
management of posterior hip dislocation
m&R with bigelow’s maneuver
- relax muscles w conscious sedation (IV fentanyl/GA/spinal)
- stabilise pelvis
- flex + upward traction + abduct + externally rotate
signs of anterior hip dislocation
abduction + external rotation + flexion of hip
management of anterior hip dislocation
m&r with barlow’s maneuver
- relax muscles
- stabilise pelvis
- flex + downward pressure + adduct + internally rotate
complications of hip dislocation
1) early
- fractures
- vascular injury
2) late
- avn of femoral head
- myositis ossificans
- coxa magna
- recurrent dislocations
- secondary OA (cartilage injury + intraarticular loose bodies)
differential diagnosis of hip pain
1) referred pain
- discogenic (sciatic nerve)
2) joint disorders
- septic arthritis
- oa
- ra
- perthe’s disease
- slipped capital femoral epiphysis
- osteonecrosis
3) bone
- fracture
- dislocation
4) periarticular disorders
- hernia
- iliotibial band tendinitis
- trochanteric bursitis
- LN
- PID
- gluteal muscle strain
- SI pathology
risk factors for avascular necrosis of hip
main: FRACTURE, DIABETES, ALCOHOL ABUSE, STEROIDS, IDIOPATHIC
V: haemoglobinopathies (e.g. sickle cell)
I - septic arthritis
T - fracture/dislocation
A - SLE, RA
M - alcohol abuse > hyperlipidemia, obesity, smoking, caisson’s disease, gaucher’s disease, cushing’s disease
I - steroids
N - malignant infiltration (leukemia/lymphoma)
C - perthes, scfe, factor v leiden
pathophysiology of avascular necrosis
1) metabolic factors
2) local factors
- arterial supply interruption/vascular damage
- venous stasis/occlusion
- capillary compression (2ndary to marrow swelling)
> increase interosseous pressure > ischaemia
most reliable modality in picking up AVN
MRI
T1: low density area (edema)
T2: double line sign
- high intensity inner line: reparative granulation tissue
- low intensity peripheral line: sclerotic bone
staging system for avascular necrosis of hip
ficat arlat (mri + xr + clinical)
ficat arlat stage 0
preclinical: at risk
normal imaging
ficat arlat stage 1
preradiographic: bone death within 48h without structural changes
- s/s: pain
xr+ ct = normal
mri = edema
bone scan = increased uptake
ficat arlat stage 2
precollapse: repair and early structural failure
- s/s: pain, stiffness
xr = sclerosis + cyst formation
mri = geographic defect
bone scan = increased uptake
ficat arlat stage 3
collapse: major structural collapse of necrostic bone
- s/s: pain, stiffness, limping
xr = crescent sign + flattening of femoral head mri = crescent sign + cortical collapse
management for ficat arlat stage 1 and 2
1) conservative
- non pharmacological: bed rest, physiotherapy, splintage, weight relief (crutches)
- pharmacological: NSAIDs, bisphosphonates
2) surgical
- core decompression + bone grafting (indication: avn from venous stasis/marrow edema)
management for ficat arlat stage 3
surgical
- femoral head resurfacing
- hemiarthroplasty
- transtrochanteric rotational osteotomy
- realignment osteotomy
ficat arlat stage 4
osteoarthritis: articular destruction
- s/s: v painful, stiffness, limp
xr = LOSS mri = 2ndary degenerative changes
management for ficat arlat stage 4
surgical
- resurfacing arthroplasty
- THR
differentials for hip pain in child <3 yo
1) infection
2) trauma
3) toddler’s fracture (1-4)
differentials for hip pain in child 3-7 yo
1) transient synovitis (3-10)
2) inflammatory/septic arthritis
3) growing pain (4-5 + puberty)
4) leukemia (4-10)
differentials for hip pain in child 7-10 yo
1) perthes disease (4-8)
2) transient synovitis
differentials for hip pain in >10 yo
1) SCFE (15)
2) growing pains
differentials for painless limb length discrepancy
1) bone
- femur vs tibial shortening
2) joint
- DDH
3) generalised
- muscle hypertrophy on one side
4) physiological
- metatarsal adductus
- tibial torsion
- femoral anteversion
- flat foot
definition of developmental dysplasia of hip
disorder of abnormal development resulting in dysplasia, subluxation and possible dislocation of hip secondary to capsular laxity & mechanical instability
epidemiology of DDH (F/M + L/R)
F>M= 6:1
L (60%) > R
risk factors for DDH
1) family history - joint laxity/shallow acetabulum
2) intrauterine malpositioning
- first born
- oligomenorrhea
- fibroids
- large baby/small mother
- breech delivery
3) post natal posture
- carrying baby with hip and knee fully extended
diagnosis for DDH in newborns
positive barlow’s + ortolani
u/s earliest at 6 weeks for high risk cases
why cant you ultrasound newborns at birth for DDH
maternal hormones facilitate emergence from birth canal > laxity of joint > inaccurate reading
diagnosis for DDH in child > 4 mths
clinical signs + XR
- positive trendelenburg test
- galleazi’s test - femoral shortening
- barlow’s test - aDduct; dislocatability
- ortolani’s test - aBduct; reducibility
radiological findings for >4mth for DDH
XR
- shallow + sharply sloping roof of acetabulum
- femoral head: small + underdeveloped + posterosuperiorly dislocated
- shenton’s line broken
- perkin’s line: epiphysis not medial
- hilgenreiner’s line: epiphysis not inferior
- acetabular index (N: <30)
- van rosen’s line = hip abducted > femoral shafts should point towards acetabulum
- medial gap: larger gap = larger possibility for dislocation
management of DDH in 0-6mth old
reducible: pavlik’s harness
irreducible : adductor tenotomy (closed reduction + hip spica)
management of DDH in 6-18 mth old
closed reduction + MUA
- successful reduction: hip spica + abduction splint
- unsuccessful reduction: open reduction (femoral derotating + shortening) > hip spica
management of DDH beyond 18 mths
salter osteotomy
- redirection of acetabulum so its roof covers femoral head both anteriorly and superiorly
complications of unreduced DDH
1) partial dislocation + pseudoarthrosis
- progressive deformity, disability + secondary OA
2) complete dislocation
- trendenlenburg gait > scoliosis
3) bilateral dislocaiton
- waddling gait > lordosis
commonest cause of hip pain in children
transient synovitis
postulated cause of transient synovitis
URTI/pharyngitis/bronchitis/otitis media
signs of transient synovitis
- most sensitive test: log roll > involuntary muscle guarding of one site
- antalgic gait
- tenderness on palpation
- mild restriction of ROM
investigations for transient synovitis
1) imaging
a. u/s joint effusion - TRO septic arthritis(infection less likely if effusion observed)
b. xr - no changes
2) lab
- WBC, CRP (tro septic arthritis), esr
management for transient synovitis
conservative
- nonpharma: heat, massage, bed rest
- pharma: NSAIDs (naproxen/ibuprofen)
risk factors of septic arthritis in children
1) prematurity
2) caesarian section
3) h/o invasive procedures
mechanism of septic arthritis
1) direct innoculation
2) haematogenous seeding (URTI precedes 80% of cases)
3) extension from adjacent bone (OM)
- neonates may have transphyseal vessels that allow spread into joint
joints with intra articular metaphysis
hip, shoulder, elbow, ankle
most common pathogen in septic arthritis
s. aureus
position of comfort in septic arthritis
FABER
progression of inflammatory markers in septic arthritis
fever > crp > esr > refusal to weight bear > wbc
investigations for septic arthritis
1) imaging
- AP + frog leg pelvis XR: widening of joint space (significant pus), subluxation/dislocation of femur
- U/S
- screen contralateral hip in neonate
- guide joint aspiration
2) lab
- FBC: wbc, esr, crp
- hip aspirate - wbc, gram stain + c/s
management of septic arthritis in children
1) conservative (rarely indicated)
- IV antibiotics (adolescent n.gonorrhea may be amenable to large dose penicillin without surgical debridement for NON HIP joint
2) surgical (*)
- urgent surgical I&D + IV antibiotics
- traction in abduction until infection resolves
complications of septic arthritis in children
1) growth disturbance
- LLD
2) femoral head destruction/deformity
3) AVN
common organisms + septic arthritis antibiotic treatment in <3mth
1st gen cephalosporin
organisms: group B strep, s. aureus, gram neg bacilli
common organisms + septic arthritis antibiotic treatment in 3mth -5 years
2nd or 3rd gen cephalosporin
organisms: s. aureus, kingella, s.pneumoniae, group A strep, h.influenzae
common organisms + septic arthritis antibiotic treatment in 5-12 years
1st generation cephalosporin
organism: s. aureus
common organisms + septic arthritis antibiotic treatment in 12-18 years
2nd or 3rd gen cephalosporin
organisms: n.gonorrhea, s.aureus
define perthes disease
idiopathic avascular necrosis of proximal femoral epiphysis in children
epidemiology of perthes (F/M + L/R)
M>F = 4:1
L=R
pathology of perthes disease
trauma/nonspecific synovitis > effusion in hip joint > pressure on lateral epiphyseal vessels in retinacula > AVN
name the classification for stages of perthes disease
waldenstrom classification
stages of perthes disease
1) initial
2) fragmentation
3) reossification
4) healing or remodelling
stage 1 of perthes disease
initial
- smaller sclerotic epiphysis
- medial joint space widening
stage 2 of perthes disease
fragmentation
- crescent sign: subchondral lucent line
- result of revascularization process with bone resorption producing collapse with subsequent patchy density and lucencies
stage 3 of perthes disease
reossification
- new bone appearance
stage 4 of perthes disease
healing or remodelling
- femoral head remodels until skeletal maturity
prognostic classification for perthes disease
catteral classification
grade 1 catteral classificaiton
involves anterior portion of epiphysis only
no collapse or sequestrum
prognosis: revascularisaiton may be complete without bone collapse
grade 2 catteral classification
<50% epiphyseal involvement with sequestrum
prognosis: bony collapse inevitable
grade 3 catteral classification
75% epiphyseal involvement with collapse and sequestrum
prognosis:
- bony collapse inevitable
- poor prognosis
grade 4 catteral classification
whole epiphyseal involvement
prognosis
- bony collapse inevitable
management of perthes disease
1) conservative (children < 8yo)
- observation + activity limitation + physiotherapy
2) surgical
- varus osteotomy of femur
- innominate osteotomy of pelvis
most common cause of hip pain in adolescents
slipped capital femoral epiphysis
risk factors of SCFE
- obesity
- acetabular retroversion + femoral retroversion
- precocious puberty
what conditions is SCFE associated with
1) endocrinopathies (bilateral SCFE)
- hypothyroidism
- hypogonadism (physeal fusion)
- hypopituitarism
- growth hormone disturbance (bone growth)
2) down’s syndrome
3) h/o trauma (30%)
pathophysiology of SCFE
stress fracture through hypertrophic zone of epiphyseal growth plate
- metaphysis translates anteriorly and externally rotates
- epiphysis remains in acetabulum
- AVN
- chondrolysis > early onset OA
signs of SCFE
- coxa vara
- shortened limb + externally rotated + fixed
= limited abduction + internal rotation - pain on movement
complications of SCFE
1) AVN
2) contralateral hip SCFE (most common complication after unilateral surgical fixation)
3) coxa vara deformity
4) chondrolysis > 2ndary OA
management of SCFE
operative
- percutaneous insitu fixation w single cannulated screw
why is maniputlation contraindicated in SCFE
increased risk of AVN
relevant history to be taken from patient presenting to the ED with open fracture
AMPLE
1) allergies
2) medications: anticoagulants, cardiovascular medication, insulin
3) past medical and surgical history
4) last meal: time of last meal to decide whether interventions needed for safe surgical intervention
5) events/environment surrounding injury
- circumstances that the injury took place
(vehicle/people involved, speed collided vehicles moving at, location of injury)
- what measures have been taken during the transfer
how would you manage a patient in shock post TKR?
1) alert on call team + senior on duty
2) STAT ECG and cardiac enzymes to evaluate for AMI
3) check knee drain for excessive blood loss + input and output charts for decreased urinary output
if decreased output:
1) order STAT FBC to check for excessive blood loss and guide management
2) renal panel for acute kidney injury
3) lactate and ABG to assess for lactic acidosis > severity of shock
4) GXM if patient require blood transfusion
if investigations point towards cardiogenic cause
1) inform on call cardiology team
2) aspirin, nitrates, analgesia according to WHO pain ladder
3) arrange for urgent PCI
if investigations rule out cardiogenic cause
- IV fluid resuscitation, blood transfusion if Hb < 7g/dL
- direct pressure on wound if active bleeding
possible causes of shock post TKR
1) cardiogenic shock (any risk factors?)
2) hypotensive shock from bleeding
principles of management in operating theatre for open fractures
1) aggressive debridement of necrotic tissue and extensive irrigation
2) fractures stabilisation (open reduction, internal/external fixation)
3) soft tissue coverage and wound closure
4) antibiotic beads placement in open dirty wounds
why is sensation over thenar eminence spared in carpal tunnel?
palmar cutaneous branch of the median nerve travels superficial to the flexor retinaculum
aetiologies of carpal tunnel syndrome
1) anatomical
- traumatic carpal fractures/dislocation
- tenosynovitis secondary to repeated hand movements (occupational work factors like awkward hand positions, hand arm vibration during construction work)
2) physiological
- fluid imbalances: pregnancy, menopause, cardiac/renal failure, obesity, hypothyroid, amyloidosis
- inflammatory: RA, GA
- metabolic: gout
- neuropathic: dm, alcoholism
- endocrine: hypothyroidism
3) idiotpathic!
causes of tardy ulnar nerve palsy
1) medial and lateral condylar fractures
2) monteggia fracture
limb attitude post proximal femoral fracture
flexed, abducted, externally rotated
limb attitude post posterior dislocation of hip
flexed, adducted, internally rotated
limb attitude post anterior dislocation of hip
flexed, abducted, externally rotated
describe management of intertrochanteric/subtrochanteric fracture in 80 year old lady
1) pre op:
- analgesic according to WHO pain ladder
- management of co morbidities
2) operative
- PFN
3) post operative
- dvt prophylaxis
- early mobilisation
why is fracture fixation preferred choice of treatment in intertrochanteric/subtrochanteric fractures (rather than hip replacement) ?
- allows for early mobility and return to premorbid function
- lower mortality rate
- improved quality of life for patient
investigations for frozen shoulder
1) XR: TRO glenohumeral arthritis, dislocation, surgical hardware
2) MRI: tro rotator cuff tear
causes of positive trendenlenburg test
1) fulcrum problems: hip OA, AVN, dislocation
2) lever arm (femoral neck) problems: NOF #, coxa vara, shortening above greater trochanter
3) muscular problems: weak abductors
4) nerve problems: superior gluteal nerve or L5
size of microfilament used in protective sensation test
5.07 gauge (applies 10g of force)
investigations to order for diabetic foot
1) biochemical
- fbc: twc
- esr, crp
- renal panel
- HbA1C (n=4-7%, indicator of diabetic control over last 3 months
- hypocount (4-8mmol/l)
- urinanalysis: glucosuria, ketonuria (DKA), proteinuria (nephropathy)
- hb: nutritional status
- culture (blood/ulcer swab)
2) imaging
- ecg, cxr (anaesthetic fitness)
- XR foot/ankle AP + lateral
- mri (differentiate abscess from st swelling)
3) vascular assessment
- ABI/TBI
- angiogram (renal function?)
cut off for ABI
normal: 1-1.2
ischaemia: <0.8
mid to mod disease: 0.5-0.9
severe disease: <0.5
critical ischaemia: <0.3
cut off for TBI
normal: >0.7
ischaemia: 0.4 -0.6
critical ischaemia: <0.3
volume of effusion tested in each of the knee effusion examinations
normal: <5cc
bulge test: 10-20cc
patella tap: 30-50cc
cross fluctuance: >60cc
investigations ordered for knee OA
1) imaging
XR: weight bearing AP, lateral, skyline + long film to look at degree of varus/valgus deformity
2) bloods
- fbc, csr, esr (inflammatory/infection)
- renal and liver panel (if giving patients NSAIDs for LT use)
associated fractures with ankle ligament injuries
1) base of 5th MT
2) lateral side of talus
3) posterior or tip of lateral and medial malleolus
4) undisplaced fibular fracture or diastasis of tibiofibular syndesmosis
imaging to order for ligament tear
1) XR
- ap
- lateral
- mortise (30 deg oblique) + talar tilt test (articular surface of tibia and talus parallel?)
- any associated fractures?
management for torn ankle ligament
1) grade I and II tears
- RICE
- bandage/brace > begin physio > protective weight bearing w crutches stopped when patient can walk > return to play
2) grade III
- RICE
- brace with hinged knee orthosis + crutches > physiotherapy > return to play
(previously BK cast immobilization from knee to toes in plantigrade)
3) operative repair in athletes - arthroscopic debridement or ligament reconstruction
management of patient with diabetic ulcer
1) general management
a. IV antibiotics: broad spectrum (augmentin + ciprofloxacin) > culture specific antibiotics
b. maintain patient’s hydration status with IV saline + monitor intake/output charts
c. daily wound dressing with chlorhexidine, flush with H2O and saline > chlorhexidine dressing
d. elevate leg if swollen
e. diabetic chart using hypocount TDS
2) i would like to classify the ulcer according to wagner’s classificaiton to better manage the patient
how would you classify diabetic ulcer?
wagner’s classifcation
describe wagner’s classification for diabetic ulcers
grade 0:
- no ulcer in high risk foot
- conservative: education, foot wear, regular exams
grade 1:
- superficial ulcer involving full skin thickness but no underlying tissues/no infection
- conservative: total contact cast for offloading + walking brace + special foot wear
grade 2:
- deep ulcer, penetrating to ligaments and muscle but no bone involvement or abscess formation
- surgical debridement + wound care + offloading + culture specific antibiotics
grade 3:
- deep ulcer with infection of deep tissue with pus; cellulitis, deep abscess tendinitis, OM
- surgical debridement/partial amputation, offloading, culture specific antibiotics
grade 4:
- forefoot gangrene
- lower extremity amputation, vascular consultation
grade 5:
- whole foot gangrene
- major extremity amputation, vascular consultation
