Etiology 5
•multifactorial
• genetic:autosomal dominant, Black children at highest risk
cartilaginous physis hypertrophies too rapidly under gr
overweight:mechanicalstress
• trauma: causes acute slip
•risk factors: obesity (No.l factor), male, hypothyroid, growth hormone deficiency, previous radiation
to hip region,renal osteodystrophy, Down Syndrome
|
=
owth hormone effects
Figure 51. Salter-Harris classification
of epiphyseal injury
Clinical Features
•acute:sudden,severe pain with limp, less than 3 wk duration
•chronic: typically groin and anterior thigh pain, may present with knee pain
• positive T rendelenburg sign on affected side, due to weakened gluteal muscles
•can be associated with knee pain due to activation of the medial obturator nerve
•restricted internal rotation, abduction, flexion
Drehmann sign:obligator)'external rotation during passive flexion of hip
•Loder classification:stable vs. unstable (provides prognostic information)
• stable = able to bear weight, with or without crutches (risk of osteonecrosis <10%)
• unstable = unable to ambulate even with crutches (high-risk of osteonecrosis, between 24-47%)
Bilateral involvement occurs In about
25%
Klein's Line
On AP view, line drawn along superolateral border of femoral neck should
cross at least a portion of the femora!
epiphysis. If it does not.suspect SCFE
Investigations
•x-ray: AP, frog-leg lateral radiographs both hips
• posterior and medial slip of epiphysis
disruption of Klein's line
AP view may be normal or show widened/lucent growth plate compared with opposite side
Treatment
•operative: percutaneous in-situ fixation without reduction (reduction is highly controversial)
•consider prophylactic fixation of contralateral hip in high-risk patients
Complications
•z\VN, chondrolysis (loss of articular cartilage,resulting in narrowing of jointspace), pin penetration,
premature OA, loss of ROM, contralateral SCFE
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Developmental Dysplasia of the Hip
Definition
• abnormal development of hip, resulting in shallow acetabulum (dysplasia), displacement with some
remaining contact between the articularsurfaces (subluxation), or complete displacement of the joint
(dislocation)
• most common orthopaedic disorder in newborns
• all newborns require screening with physical exam
Etiology
• due to ligamentous laxity, muscular underdevelopment, and abnormal shallow slope of acetabular
roof
• spectrum of conditions
• dysplastic acetabulum, more shallow, and more vertical than normal
head subluxates out of joint when provoked
• dislocatable head in socket
dislocated femoral head completely out of acetabulum
Physical Exam
• diagnosis is clinical
limited abduction of the flexed hip (<60°)
affected leg shortening results in asymmetry in skin folds and gluteal muscles, wide perineum
Barlow’
s test demonstrates whether hips are dislocatable
flex hips and kneesto 90° and grasp thigh
fully adduct hips, push posteriorly to try to dislocate hips,feeling for a distinct clunk
Ortolani’s test demonstrates whether hips are reducible
initial position as above but try to reduce hip with fingertips during abduction
positive test: palpable clunk is felt (not heard) if hip is reduced
T rendelenburg test and gait useful if older (>2 yr)
Cialeazzi'
s sign
knees at unequal heights when hips and knees flexed
appearance of a shorter femur (lower knee) on affected side
difficult test if child <1 yr
Investigations
• perform screening U/S at 4-6 weeks in patients with risk factors and positive physical findings to view
cartilage (bone is not calcified in newborns until 4-6 mo)
• follow-up radiograph after 3 mo
• x-ray signs (at 4-6 mo):false acetabulum, acetabular index >25°, broken Shenton’
sline,femoral neck
above Hilgenreiner’
s line (horizontal line through right and left triradiate cartilage),ossification
centre outside of inner lower quadrant (quadrantsformed by intersection of Hilgenreiner’
s and
Perkin’
slines)
Barlow'
stest
lv\
i
®
Ortolani'
s tost
Figure 52. Barlow’s test and
Ortolani's test
(
*3
5 Fs that Predispose to Developmental
Dysplasia of the Hip
Fanily history
Female
Frank breech
First born
LeFt hip Treatment
• 0-6 mo:reduce hip using Pavlik harness to maintain abduction and flexion
• 6-18 mo: reduction under GA, hip spica cast x 2-3 mo (if Pavlik harness fails)
• 18 nio-2 yr: open reduction with spica casting
• >2 yr: pelvic and /or femoral osteotomy
Complications
• redislocation, inadequate reduction,stiffness
• AVN of femoral head may be seen at any point in treatment; due to impingement of medial circumflex
femoral artery with severe abduction and flexion secondary to prolonged Pavlik harness or spica cast
treatment
Legg-Calve-Perthes Disease (Coxa Plana)
Most common in adolescent athletes,
especially jumping/sprinting sports
Definition
• idiopathic AVN of femoral head, presents at 4-8 yr of age
. 12% bilateral, M:P=5:1, 1/1200 children
• associations
family history of Legg-Calve-Perthes Disease
low birth weight
abnormal pregnancy/delivery
• ADHD in 33% of cases, delayed bone age in 89%
second-hand smoke exposure
• key features
» AVN of proximal femoral epiphysis, abnormal growth of the physis, and eventual remodeling of
regenerated bone
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Children diagnosed with coxa plana
<6 yr of age have improved prognosis
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0R18 Orthopaedic Surgery Toronto Notes 2023
Clinical Features
• child tvith antalgic or T rendelenburg gait ± pain
• intermittent knee, hip, groin, or thigh pain
• flexion contracture (stiff hip)
• decreased internal rotation and abduction of hip
• limb length discrepancy (late)
Investigations
• x-ray: AP pelvis,frog leg lateral
• initially, may be negative; if high index of suspicion, obtain bone scan or MR1
• eventually, collapse of femoral head will be seen (diagnostic)
Figure 53.Pelvic x-ray and reference
lines and angles for assessment of
DDH
TriradiateCartilage
y-shaped epiphyseal plate at junction
of ilium,ischium,and pubis
Hilgenreiner’sLine
Line running between triradiate
cartilages
Perkin's Line
Line through lateral margin of
acetabulum,perpendicular to
Hilgenreiner's Line
Shenton’sLine
Arced line along Inferior border of
femoral neck and superior margin of
obturator foramen
Acetabular Index
Angle between Hilgenreiner's Line
and line from triradiate cartilage to
point on lateral margin of acetabulum
Treatment
• goal is to keep femoral head contained in acetabulum and maintain ROM (contain and maintain)
• non-operative
physiotherapy: ROM exercises
restricted weightbearing
• operative
« femoral or pelvic osteotomy (>8yr of age orsevere)
prognosis better in males, <6 yr, <50% of femoral head involved, abduction >30°
• 60% of involved hips do not require operative intervention
• natural history is early onset OA and decreased ROM
Osgood-Schlatter Disease
Definition
• inflammation of patellar ligament at insertion point on tibial tuberosity
. M>F; boys 12-15 yr;girls 8-12 yr
Mechanism
• repetitive tensile stress on insertion of patellar tendon over the tibial tuberosity causes minor avulsion
at the site and subsequent inflammatory reaction (tibial tubercle apophysitis)
Clinical Features
• tender lump over tibial tuberosity
• pain on resisted leg extension
• anterior knee pain exacerbated by jumping or kneeling, relieved by rest
Investigations
• x-ray lateral knee:fragmentation of the tibial tubercle,± ossicles in patellar tendon
Treatment
• benign,self-limited condition, does not resolve until growth halts
• non-operative (majority)
• avoid aggravating activitiessuch as basketball or cycling
NSAJDs, rest, flexibility, isometric strengthening exercises
casting ifsymptoms do not resolve with conservative management
• operative:ossicle excision in refractory cases (patient is skeletally mature with persistent symptoms)
Congenital Talipes Equinovarus (Club Foot)
Definition
• congenital foot deformity
• muscle contractures resulting in CAVE deformity
• bony deformity: talar neck medial and plantar deviated;varus calcaneus and rotated medially around
talus; navicular and cuboid medially displaced
Etiology
• intrinsic causes (neurologic, muscular, or connective tissue diseases) vs. extrinsic (intrauterine
growth restriction);maybe idiopathic, neurogenic,orsyndrome-associated
• fixed deformity
• 1-2 in 1000 newborns, 50% bilateral, M>F-2:1,severity 1
;
>M
Physical Exam
• examine for CAVE deformity
• examine hips for associated DDH
• examine knees for deformity
• examine back for dysraphism (unfused vertebral bodies)
• diagnosis is often from physical exam findings alone, radiographs unnecessary
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CAVE deformity
Midfoot Cavu (tight intrinsics, FHL,FDL)
Forefoot Adductus (tight tibialis
posterior)
Hindfoot Varus tight Achilles tendon,
tibialis posterior,tibialis anterior)
Hindfoot Equinus (Hindfoot Equinus
(tight Achilles tendon)
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Treatment
• largely non-operative via Ponseti Technique (serial manipulation and casting)
• correct deformities in CAVE order
change strapping/cast ql-2 wk
typically requires percutaneous Achilles tendon release after ~ 2 months of casting with
another 3 weeks of casting in maximal dorsiflexion
surgical release in refractory case (rare)
• delayed until age 3-4 mo
• 3 yr recurrence rate = 5-10%
• mild recurrence common;affected foot is permanently smaller/stiffer than normal foot with calf
muscle atrophy
' Plantar flexion
of ankle joint
Talus in equinus
and varusI
v, I
0
[0
/
-j
I1
Forefoot
bones in
varus,
Inversion of i
calcaneus Scoliosis
Figure 54.Club foot
- depicting the
Definition gross and bony deformity
• lateral curvature ofspine with vertebral rotation
• age:10-14 yr
• more frequent and more severe in females
Etiology
• idiopathic: most common (90%)
• congenital:vertebrae fail to form orsegment
• neuromuscular: UMN or LMN lesion, myopathy
• postural:leg length discrepancy, muscle spasm
• other: osteochondrodystrophies, neoplastic, traumatic
Clinical Features
• cosmetic concern ± back pain
• primary curve where several vertebrae affected
• secondary compensatory curves above and below fixed primary curve to try to maintain normal
position of head and pelvis
• asymmetric shoulder height when bent forward
• Adam’
s test: thoracic or lumbar prominence on affected side with forward bend at the waist
• prominent scapulae, creased flank, asymmetric pelvis
• associated posterior midline skin lesions in neuromuscular scoliosis
• cafe-au-lait spots, dimples, neurofibromas
• axillary freckling, hemangiomas, hair patches
• associated pes cavus or leg atrophy
• apparent leg length discrepancy
• Scoliosis Lenke Classification: guide to select curves to be included within the fusion construct
Figure 55.Cobb angle -
used to monitor the progression of
the scoliotic curve
Investigations
• x-ray:3-footstanding, AP, lateral
measure curvature:Cobb angle
• may have associated kyphosis
Scoliosisscreening is not recommended
in Canada (Grieg A,et al.2010; Health
Canada.1994)
Treatment
• based on Cobb angle
• <25°: observe for changes with serial radiographs
• >25° or progressive:bracing (many types, controversial) that halt/slow curve progression but do
not reverse deformity
• >45°, cosmetically unacceptable, or respiratory problems:surgical correction (spinal fusion)
In structural or fixed scoliosis, bending
forwards makesthe curve more obvious
Postural scoliosis can be corrected by
correcting the underlying etiology
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Bone Tumours
•primary bone tumours are rare after 3rd decade
•metastasesto bone are relatively common after 3rd decade
Clinical Features
•malignant (primary'or metastasic):local pain and swelling (weeks to months), worse on exertion and
at night, ± soft tissue mass
•minor trauma can be the initiating event that calls attention to lesion
Red Flags
• Persistentskeletal pain
• Localized tenderness
• Spontaneousfracture
• Enlarging mass
-soft tissue swelling
Table 25. Distinguishing Benign from Malignant Bone Lesions on X-Ray
©
Benign Malignant
No periostealreaction or benign appearing reaction (e.g.uniform
smooth periosteal thickening as seen ina healing fracture)
Acute periosteal reaction
•Codman’s triangle
•"Onion skin"
•"Sunburst”
Poorly defined borders,with a wide zone of transition,orinfiltrative
(suggesting fast-growing lesion)
Varied bone formation
Eitraosseousand irregular calcification
Soft tissue mass present
Aggressive cortical destruction or tumour infiltration without cortical
destruction
Describing Bone Tumours on X-rays
1 Location (which bone and whether
it isin the diaphysis.metaphysis.or
epiphysis)
Sharp,well-demarcated borders,narrow zone of transition (between
lesion andnormal bone,suggesting slow-growing lesion)
Well-developed bone formation
Intraosseous and even calcification
No soft tissue mass
No cortical destruction or uniform cortical destruction in some low
grade and locally aggressive benign lesions
2 Size
3 Solitary vs.multifocal
4 Morphology:geographic,permeative,
or moth-eaten margins
5 Presence of periosteal reaction
6 Presence of bony remodeling
7 Cortical involvement
8 Matrix:osteoid (cumulus cloud),
chondroid (punctate or popcorn
calcification),or fibrous (ground glass
appearance)
9 Presence of soft-tissue mass
10 Associated pathological fracture
Adapted from Bucktioltz RW. Heckman JD.Rockwood and Green'
s Fractures in Adults.Volume1. Philadelphia: Uppincotl Williams & Wilkins.2001.
p558
Diagnosis
• malignancy issuggested by rapid growth, warmth, tenderness, aggressive features on imaging
• may be associated with constitutional symptomssuch as fevers, night sweats, weight loss,or loss of
appetite
• staging should include:
• local
full length radiographs of the affected bone
± CT and/or MR1 of affected bone
biopsy
should be referred to specialized centre for biopsy
• systemic
blood work (CBC, electrolytes,liver function assays, inflammatory markers,bone profile,
extended electrolytes including calcium)
serum electrophoresis for older patients ± Bence )ones protein
CT chest/abdo/pelvis
Bone scan or bone marrow biopsy depending on preliminary diagnosis
Neoplasi
Periosteum
Benign Active Bone Tumours
Codman'
s
triangle BONE-FORMING TUMOURS .1
Figure 56. Codman’s triangle
A radiographic finding in
malignancy,where the partially
ossified periosteum islifted off the
cortex byneoplastic tissue
Osteoid Osteoma
• benign bone tumour arising from osteoblasts; not known to metastasize
• peak incidence in 2nd and 3rd decades, M:F=2-3:1
• proximal femur>tibia diaphysis most common locations;spine (can cause painfulscoliosis)
• radiographic findings:small, round radiolucent nidus (<1.5 cm) surrounded by dense sclerotic bone
(
"
bulf'
s-eye” )
• symptoms: constant and progressive pain from prostaglandin secretion and COXI/2 expression
• pain worse at night (diurnal prostaglandin production); characteristically relieved by NSAIDs
• treatment: NSAIDs are first-line; percutaneous radiofrequenev ablation or surgical resection for
refractory lesions
FIBROUS LESIONS
Fibrous Cortical Defect (i.e. non-ossifying fibroma, fibrous bone lesion)
• developmental defect in which areas that normally ossify are filled with fibrous connective tissue
• most common benign bone tumour in children,typically asymptomatic and an incidental finding
• occur in as many as 35% of children, peak incidence between 2-25 yr old
• distal femur > distal tibia > proximal tibia most common locations
• radiographic findings:diagnostic, metaphyseal eccentric ‘bubbly’ lytic lesion near physis;thin,
smooth/lobulated, well-defined sclerotic margin
• multiple lesions can be present;large lesions may be associated with pathologic fractures
• treatment: most lesions resolve spontaneously;curettage and hone grafting for symptomatic lesions or
to prevent pathologic fractures in larger lesions
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Osteochondroma
• cartilage capped bony lesion arising on the external surface of a bone
• 2nd and 3rd decades, M>1
:
• most common benign bone tumour (~30%); true incidence unknown as many asymptomatic
• 2 types:sessile (broad based and increased risk of malignant degeneration) vs. pedunculated (narrow
stalk)
• metaphysis of long bone near tendon attachment sites(distal femur, proximal tibia, or proximal
humerus)
• radiographic findings: cartilage-capped bony spur on surface of bone (“mushroom"
on x-ray)
• may be multiple (hereditary, autosomal dominant form)
- higher risk of malignant change
• generally very slow growing and asymptomatic unless impinging on neurovascularstructure
(‘painless mass’)
growth usually ceases when skeletal maturity is reached
• malignant degeneration occursin 1-2% (becomes painful or rapidly grows)
• treatment: observation;surgical excision ifsymptomatic or concern for malignant transformation
Enchondroma
• benign hyaline cartilage growth; abnormality of chondroblasts, develops in medullary cavity
single/multiple enlarged rarefied areas in tubular bones
lytic lesion with sharp margination and irregular central calcification (stippled/punctate/popcorn
appearance)
• majority asymptomatic, presenting as incidental finding or pathological fracture
• 2nd and 3rd decades
• 60% occur in the small tubular bones of the hand and foot; others in femur (20% - Figure 57),
humerus, ribs
• radiographic findings:well-defined,lucent, central medullary lesions that calcify over time
• malignant degeneration to chondrosarcoma occurs in 1-2% (rest/nocturnal pain in absence of
pathologic fracture is an important clue)
• treatment: observation with serial x-rays;surgical curettage if symptomatic or lesion grows
Figure 57. T1MRI of femoral
enchondroma
CYSTIC LESIONS
Unicameral/Solitary Bone Cyst
• most common cystic lesion;serousfluid-filled lesion with fibrouslining
• children and young adults, peak incidence during first 2 decades
• proximal humerus and femur most common
• symptoms: asymptomatic, or localized pain; complete pathological fracture (50% of presentations) or
incidental detection
• radiographic findings:lytic translucent area on metaphyseal side of growth plate, cortex thinned/
expanded; well-defined lesion
• treatment:observation with serial radiography 4-6 mo;if needed, aspiration followed by steroid
injection; curettage ± bone graft indicated if structural integrity of bone is compromised
Benign Aggressive Bone Tumours
Giant Cell Tumours/Aneurysmal Bone Cyst/Osteoblastoma
• affects patients of skeletal maturity, peak 3rd decade
• osteoblastoma: most commonly found in posterior elements of spine
• giant cell tumour: pulmonary metastases in 3%
• aneurysmal bone cysts: either solid with fibrous/granular tissue, or blood-filled
• radiographic findings
• giant cell tumour: eccentric lytic lesions in epiphyses adjacent to subchondral bone; may break
through cortex;T2 MRI enhances fluid within lesion (hvper-intense signal)
aneurysmal bone cyst:expansile, eccentric,and lytic lesion with bony septae (“bubbly
appearance"); will have fluid-fluid levels on MRI
osteoblastoma:often nonspecific; calcified central nidus (>2 cm) with radiolucent halo and
sclerosis
• symptoms: local tenderness and swelling, pain may be progressive (giant cell tumours), ± symptoms
of nerve root compression (osteoblastoma)
Treatment
• intralesional curettage + bone graft or cement
• wide local excision of expendable bones
• recurrence rates of up to 20%
Figure 58. X-ray of aneurysmal bone
cyst
Note the aggressive destruction of
bone
Figure 59. X-ray of osteosarcoma of
distal femur
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n
Malignant Bone Tumours
Table 26. Most Common Malignant Tumour Types for Age
Age Tumour
«1 Neuroblastoma
Ewing’s ol tubular bones
Osteosarcoma. Ewing'
s ol Hat bones
Reticulum cell sarcoma,fibrosarcoma, periosteal osteosarcoma,malignant giant cell tumour, lymphoma
Metastatic carcinoma, multiple myeloma, chondrosarcoma
1-10
10-30
30 40
>40
Osteosarcoma
• malignant bone tumour
• 2nd most common primary malignancy in adults after myeloma
• majority occur in 2nd decade oflife,second peak in elderly patients with history of Paget’s disease
• predilection forsites of rapid growth:distal femur (45% -Figure 59,OR51 ),proximal tibia (20%), and
proximal humerus(15%)
• invasive, variable histology;frequent metastases without treatment (lung most common)
• painful symptoms: progressive pain, night pain, poorly defined swelling, decreased ROM
• radiographic findings: characteristic blastic and destructive lesion (“sunburst"
pattern),
periosteal reaction (Codman's triangle),soft tissue mass with maintenance of bone cortices;
destructive lesion in metaphysis may cross epiphyseal plate
• bone scan -rule outskeletal metastases; CT chest-rule out pulmonary metastases
• treatment:staging, neo-adjuvant chemotherapy, re-staging, limb salvage resection/reconstruction
(rarely amputation), post-surgical neo-adjuvant chemotherapy
• prognosis:90% survival forlow-grade; 70% survival for high-grade
Chondrosarcoma
• malignant chondrogenic tumour
• primary (2/3 cases)
• previous normal bone, patient >40 yr;expandsinto cortex to cause pain, pathological fracture
• secondary (1/3 cases)
malignant degeneration of pre-existing cartilage tumour such as enchondroma or
osteochondroma
• age range 25-45 yr, better prognosis than primary chondrosarcoma
• symptoms: progressive pain, uncommonly palpable mass or pathologic fracture
• radiographic findings:in medullary cavity, irregular "popcorn"
calcification
• treatment:no role for neo-adjuvant chemotherapy or radiation; treat with wide surgical resection +
reconstruction;regular follow-up x-rays of resection site and chest
• prognosis:90% ten-yearsurvival for low-grade; 29-55% survival for high-grade
Ewing's Sarcoma
• malignant,small round cell sarcoma; metastases frequent without treatment
• most occur between ages 5-25 yr
• tlorid periosteal reaction in metaphysis oflong bone with diaphyseal extension
• signs/symptoms: presents with pain, fever, erythema, and swelling; anemia, increased WBC, HSR,
LDH (mimics an infection)
• radiographic findings: destructive lesion with moth-eaten appearance and periosteal lamellated
pattern (“onion-skinning")
treatment:resection + chemotherapy ± radiation (can be treated solely with radiation in younger
patientsin select anatomic locations)
• prognosis: 70% survival;distant metastasessignificantly lowersurvival (<30%)
Figure 60.X-ray of femur
chondrosarcoma
Signs ol Hypercalcemia
"Bones.Stones. Moans, Groans.
Psychiatric overtones"
CNS: headache, confusion, irritability,
blurred vision
Gl: N19,abdominal pain, constipation,
weight loss
MSK:fatigue,weakness, unsteady gait,
bone and joint pain
GU:nocturia, polydipsia, polyuria, UTIs
Most Common Tumours
Metastatic to Bone
.Thyroid ,
Breast Breast
Lung Lung
^
Melanotna^
)
Kidney Kidney
Multiple Myeloma
• proliferation of neoplastic plasma cells
• most common primary bone malignancy
• 90% occur in people >40 yr; M:l-
'
=2:1; twice as common in individuals of African descent
• signs/symptoms:localized bone pain (cardinal early symptom), compression/pathological fractures,
renal failure, nephritis, high incidence of infections (e.g. pyelonephritis/pneumonia),systemic
(weakness, weight loss, anorexia)
• labs: anemia, thrombocytopenia, increased HSR, hypercalcemia, increased Cr
• radiographic findings:multiple, “punched-out” well-demarcated lesions, no surrounding sclerosis,
marked bone expansion
• diagnosis
• serum/urine immunoelectrophoresis (monoclonal gammopathy)
• CT-guided biopsy of lytic lesions at multiple bony sites
Prostate
BLT with a Kosher Pickle
Breast
Lung
Thyroid
Kidney
Prostate
n
LJ
• treatment
• multiagent chemotherapy ± stem cell transplantation ± bisphosphonates
• surgery for impending fractures: debulking, internal fixation +
• prognosis:5 yr survival 52%, prognosis increases with decreasing age
• see Hematology, H5I
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Bone Metastases
• most common cause of bone lesions in adults; typically age >40
• majority arise from breast or prostate;some arise from lung, thyroid, and kidney
• usually osteolytic lesions; prostate occasionally osteoblastic
• may present with mechanical pain and/or night pain, pathological fracture, hypercalcemia
• bone scan for MSK involvement; MR1 if suspected spinal involvement
• treatment: pain control, bisphosphonates, surgical stabilization of impending fractures if Mirel’s
Critera >8
Table 27. Mirel’s Criteria for Impending Fracture Risk and Prophylactic Internal Fixation
Variable Number Assigned
1 2 3
Site Upper arm Lower extremity Peritrochanleric
Moderate
Mixed
1/3-2Z3 diameter
Pain Mild Severe
Lesion Elastic
<1/3 bone diameter
lytic
Siie >2/3 dtamcler
Common Medications
Table 28. Common Medications
Drug Name Dosing Schedule Indications Comments
ccfazolin (Anccl ) 12 g IV qS h Preoperativcanlibiolic
prophylaxis
First generation cephalosporin;can
be used withpenicillin allergy|< t0%
cross-reactivity;significantly higher
rales olSSI/PTI with alternative ABx)
Fixed dose,no monitoring, improved
bioavailability,increased bleeding
rates
Predictable,no monitoring,oral
administration
Reversal agents:
idarucirumab(dabigatran)
andexanet alia|rivaroxaban,
apixaban)
Recent evidence suggests similar
efficacy to IMWH and Rlvaroxaban
with belter side effect profile (lower
hematoma/sliffness in TJA)
Reduce perioperative blood loss No evidence for increase in
thromboembolic events
Analgesia for pain control Max dose up to 4000 mg every 24h
Higher doses can be hepatotoxic in
susceptible individuals
S000 IUSC once daily
30- 40 mgSC once daily to BIO
2.5mg SC once daily
110 mg P0 x1then 220 mg P0
once daily
10 mg P0 once daily
2.5 mg P0 BID
IMWH 0VIprophylaxis
dalteparin (Fragmin ')
enoxaparin (Lovenox:
)
oral anticoagulants
dabigatran |Pradaxa!
)
rivaroxaban fXarelto
apixaban (Eliquis 5)
DVT prophylaxis
Aspirin (ASA) gtmgPOBIO 0VI prophylaxis
tranexamicacid(TXA) 10-20 mg/kg IV
Topical application to wound
1000mg POqGh or q8 h
and transfusion
acetaminophen (Tylenol- )
ibuprofen (Advil .Motrin ) 200-800 mg P0q6-8 Ir
(max 3200 mg/d|
Analgesia for inflammatory pain NSAID.maycause gastric erosion
(arthritis) and bleeding;avoid il concurrent
advancedrenaldisease
triamcinolone (Aristocort ')
- 0.5 -1mlol 25 mg/ml
an injectable steroid
Suspension (Injected inlo Potent anti inflammatory died;
inflamed joint or bursa);amount increased pain for 24 h.rarely
varies by joint sire causes falnetrosis and skin
depigmentalion
naproxen (Aleve -
,Naprosyns) 250-500 mg BID Analgesia for pain due to
inflammation,arthritis,soft
tissue injury
Component of multimodal pain
control and prophylaxis of HO
after THA
Prophylaxis of HO alter 1HA
NSAID.maycause gastric erosion
and bleeding;avoid if concurrent
advanced renal disease
celecoxib (Celebrex -) 200 mg P0 BID NSAID (COX-2 inhibitor),cardiotoxic
indomethacin (Indocid ) 2SmgP0IID Use with misoprostol
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Landmark Orthopaedic Trials
Trial Name Reference Clinical Trial Details
NEJM 2019:381:2199-2208 Title: Total Hip Arthroplasty or Hemiarthroplasty for Hip Fracture
Purpose:Despite being amongst the top10 causes of disability in adults,there is still ambiguity in the treatmentof displaced
femoral neck fractures.
Methods:1495 patients who were 50- years old and had a displaced femoral neck fracture were randomly assigned to have a total
hip arthroplasty or hemiarthroplasty.
Results:A secondary hip procedure within 24 months of follow up occurred in 7.9% of the total hip arthroplasty and 8.3% of the
hemiarthroplasty group.Hip Instability occurred in 4.7% ol the total hip arthroplasty,and 2.4% of the hemiarthroplasty group.
Function was modestly better in totalhip arthroplasty over hemiarthroplasty.
Conclusions: The incidence ol secondary procedures,and function over 24 months between the total hip arthroplasty and
hemiarthroplasty group did not have a significant difference.
Title:Surgical vs.Honsurgical Treatment of Adults with Displaced Fractures of the Proximal Humerus:the PROFHER Randomized
Clinical Trial
Purpose: To evaluate the efficacy of surgical management in adults with displaced fractures of the proximal humerus involving the
surgical neck.
Methods: A randomized clinical trial where 260 palienls. who presented to 32 UK hospitals alter sustaining a displaced fracture of
the proximal humerus involving the surgical neck were randomizedinto surgicaland nonsurgical lioatmcnt groups, then followed
for 2 years.
Results:No significant mean treatment group differences inOxford Shoulder Score averaged over 2 years (39.07 points for the
surgical group vs.38.32points for the nonsurgical group:difference of 0.75 points (95% Cl,-1.33 to 2.84 points);P *.48).
Conclusions:No significant differences between surgical treatmentvs.non-surgrcal treatment.These results do notsupport the
use of surgery for patients with displaced proximalhumerus fractures involving the surgical neck.
Title: A Trial of Wound Irrigation in the Initial Management of Open Fracture Wounds
Purpose: toinvestigate the effects of castile soap versus normal saline irrigation delivered by means of high, low, or very low
Irrigation pressures.
Methods: 2551palienls from 41clinical centers,who had an open fracture olan extremity undergoing irrigation were randomly
assigned to one of threeirrigation pressures (high,low, and very low) and one of two irrigationsolutions (castile soap versus normal
saline).The primary outcome in this study was reoperation within12 months after the initial surgery.
Results:Hazardratio showed no significant difference between the rates of reoperation within12 months between the different
irrigation pressures.Reoperation occurred in14.8% in the soap group and in11.6% in the saline group (hazard ratio.1.32.95%Cl,
1.06 to1.66;P-0.01).
Conclusions:Rates of reoperation were similar regardless of irrigation pressure. The reoperation rate was higher in the soap group
than in the saline group.These findings indicate low pressure saline irrigationis an acceptable form olwound irrigation.
HEALTH
PR0FHER JAMA 2015 Mar 10:313(10):1037-47
FLOW N Engl J Med 2015:373:2629 2641
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References
Acronyms
Basic Anatomy Review.
OT2 OT27
OT2 OT28
Ear
Nose
Throat
Head and Neck
Anatomical Triangles of the Neck
Differential Diagnoses of Common Presentation
Dizziness
Otalgia
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Tinnitus
Nasal Obstruction
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Types of Hearing Loss
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Speech Audiometry
Impedance Audiometry
Auditory Brainstem Response
Otoacoustic Emissions
Aural Rehabilitation
Vertiga
Evaluation of the Dizzy Patient
Benign Paroxysmal Positional Vertigo
Meniere's Disease (Endolymphatic Hydrops)
Vestibular Neuronitis (Labyrinthitis)
Acoustic Neuroma (Vestibular Schwannoma)
Tinnitus
Diseases of the External Ear
Cerumen Impaction
Exostoses
Otitis Externa
Malignant (Necrotizing) Otitis Externa (Skull Base Osteomyelitis)
Diseases of the Middle Ear.
Acute Otitis Media and Otitis Media with Effusion
Chronic Otitis Media
Cholesteatoma
Mastoiditis
Otosclerosis
Diseases of theInner Ear.
Congenital SensorineuralHearing Loss
Presbycusis
Sudden Sensorineural Hearing Loss
Autoimmune Inner Ear Disease
Drug Ototoxicity
Noise-Induced Sensorineural Hearing Loss
Temporal Bone Fractures
Facial Nerve (CN VII) Paralysis
Rhinitis.
Allergic Rhinitis (i.e.Hay Fever)
Vasomotor Rhinitis
Rhinosinusitis
Acute Bacterial Rhinosinusitis
Chronic Rhinosinusitis
OT6
OT30
OT32
OT9
OT 33
OT35
OT12 OT39
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Acronyms
ABR auditory brainstem response
AC air conduction
AOM acute otitis media
BAHA bone-anchored hearing aid
BC bone conduction
BPPV benign paroxysmal positional
vertigo
CHL conductive hearing loss
CMV cytomegalovirus
CNS central nervous system
CP cerebellopontine angle
CPAP continuous positive airway
pressure
cerebrovascular accident
external auditory canal
endoscopic sinus surgery
Epstein-Barr virus
familial adenomatous polyposis OE
fine needle aspiration
gastroesophageal reflux disease OME
granulomatosis withpolyangiitis OPC
head and neck
hearing loss
HPV human papillomavirus
herpes simplex virus
intranasal corticosteroids
middle car effusion
middle ear inflammation
multiple sclerosis
otitis externa
otitis media
otitis media with effusion
oropharyngeal cancer
obstructive sleep apnea
polymorphonuclear leukocytes
rheumatoid arthritis
RSV respiratory syncytial virus
SCC squamous cell carcinoma
SCM sternocleidomastoid
SNHL sensorineural hearing loss
SRI speech reception threshold
TEF tracheoesophageal fistula
TM tympanic membrane
TMJ temporomandibular joint
TMP-SMX trimethoprim/sulfamethoxazole
URTI upper respiratory tract infection
RA
HSV
CVA INCS
tiL MEE
ESS MEI
EBV MS
FAP
FNA OM
GERD
GPA
H&N CSA
HI PMN
Basic Anatomy Review
Ear
External
Temporalis fascia Auditory ossicles
and muscle
Middle Inner
Semicircular canals
Triangular
fossa
Helical crus
Vestibular
e r v e
— Vestibulocochlear
terve (CN VIII)
Antihelix
Cochlear
nerve
Scapha
Facial nerve (CN VIII
Cochlea
Antitragus
Lobule
Eustachian tube
HD Susan Park 2009
acoustic Tympanic
®
meatus membrane Aarti Inamdar
Figure1.Surface anatomy of the external ear;anatomy of ear
Tympanic mombrano viewed
through speculum
View into tympanic cavity after
removal of tympanic membrane
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3
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^ "
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-
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Incus long process
Stapes
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: —Long process of —H
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tendon
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> 1 muscle
Tympanic plexus
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Annulus
L tensa
Figure 2.Normal appearance of right tympanic membrane on otoscopy
r T
L J
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