Radiology Flashcards
what do we do with new fractures?
refer to orthopedist
if in cervical spine, call 911
what makes a compression fracture new?
step defect
trabecular impaction
compare to old films
What will MRI show when looking at a new fracture? CT?
marrow edema
extent of body involvement and possible comminution
what do we do with degenerative arthritides?
we manage it
consider MRI for disc evaluation and CT/MRI for spinal canal stenosis
if it gets worse, consider orthopedic/neurological consult
what do we do with inflammatory/connective tissue arthridities?
co-manage with rheumatologist. lab studies support radiographic diagnoses.
erosions could lead to instabilities
perform cervical flexion, extension views, which may refer to orthopedist
what do we do with metabolic arthridities?
co-manage with rheumatologist
what do we do with benign tumors?
co manage
benign tumors are imaged with MRI to evaluate marrow characteristics and CT to evaluate cortical bone changes. some tumors simply need monitoring for future symptom development (osteochrondroma, hemangioma).
some benign tumors weaken bone and will need to be removed to avoid complications.
refer to orthopedist
what do we do with malignant tumors?
co-manage with oncologist
MRI will evaluate for bone destruction.
CT will define the extent of cortical destruction
radionuclide scintigrophy will reaveal multiple sites of involvement
chest films will evaluate metastatic spread to the lungs
lab studies may confirm bone destruction and most likely pathology
biopsy will reveal the particular pathology
what do we do with tumor like process?
co manage with oncologist and orthopedist, similar to malignant management. paget disease and fibrous dysplasia are benign, but have malignant potential
where does OA typically occur?
disc, posterior facets, extremities
associated conditions of OA
DISH, OPLL, OCI, risks for canal stenosis
who usually gets OA?
40 and older
may be seen in limited number of post-trauma, more likely in regions of anomalous joints (SCFE, DDH, healed AVN)
management for OA
chiro care unless with hypermobility
allopath: pain meds, surgical fusion, joint replacement
does OA cause erosions or lead to fusion?
NO
findings on xray with disc disease
decreased disc height, osteophytes, intercalary ossicles, vaccum phenomenon, posterior translation of vertebra, subchondral sclerosis (eburnation), uncinate hypertrophy (lushka joint hypertrophy)
findings on xray with posterior joint disease
posterior facet hypertrophy/arthrosis, anterior translation of vertebrae (spondylolisthesis), interspinous sclerosis (baastrup’s/kissing spinous process)
types of spondylolisthesis
I: dysplastic, congenital anomalies
II: isthmic, pars interarticularis defect
III: degenerative
IV: traumatic, fracture other than pars (Hangman’s fracture)
V: iatrogenic
bony causes of spinal canal stenosis
osteophytes, paget, hemangioma (when expansile), pedicle hypoplasia, congenital anomalies
soft tissue causes of spinal canal stenosis
disc herniations, OPLL, facet capsule ossification, ligamentum flavum thickening
C2-7 discs go with which nerve roots?
C2 disc- C3 NR C3 disc- C4 NR C4 disc- C5 NR C5 disc- C6 NR C6 disc- C7 NR C7 disc- C8 NR
if there was a PARACENTRAL disc herniation in the lumbars, which nerve roots would be affected?
L1 disc- L2 NR L2 disc- L3 NR L3 disc- L4 NR L4 disc- L5 NR L5 disc- S1 NR
if there was a LATERAL disc herniation in the lumbars, which nerve roots would be affected?
L1 disc- L1 NR L2 disc- L2 NR L3 disc- L3 NR L4 disc- L4 NR L5 disc- L5 NR
people who get DISH
people who get diabetes, middle age-older, overweight, metabolic syndrome, cardiovascular disease
what should you evaluate for for people with DISH? how?
diabetes
blood or urine analysis
Can we adjust a segment with DISH?
no..
osteitis condensans ilii
most commonly seen in postpartum women, but could be seen in men
iliac-based sclerosis, importantly WITHOUT EROSIONS
if there is erosions, DDX of sacroiliitis
which OAs have erosions?
erosive OA
RA
Psoriatic
who gets these inflammatory arthridities? RA AS EA PA reactive
RA: middle aged women AS: younger men EA: younger women PA: middle aged, no gender bias reactive: younger men
what are some complications of inflammatory arthridities?
pain, erosions, ankylosis
describe RA
common, autoimmune, multisystem (joints, lungs, kidneys) disease, aggressive and progressive
describe the joints of someone with RA
hyperplastic synovitis (pannus) formation, causing symmetrical loss of joint space and erosions, usually polyarticular.
bilateral and symmetrical
prefers wrists, hands, shoulders, feet, knees, hips, cervical spine
s/s in the extremities of RA
soft tissue swelling
hands achy in the morning
hyperemia around joints leads to juxta-articular osteopenia
bare area erosions
region of RA will eventually becomes osteopenic
joint deformities
ankylosis
RA in hands, wrists, feet
usually first site of involvement bilateral and symmetrical within the body and within the involved joint MCP and PIP first swan neck deformity boutonniere deformity ulnar deviation of fingers at MCP fibular deviation of toes at MTP erosions around ulnar and radial styloid processes erosions within carpals
RA in the shoulders
erosions at AC joint, sometimes causing resorption of distal clavicle
erosions around humeral head and acromion
erosions around supraspinatus tendon leading to rotator cuff tear, which results in elevation of the humeral head and reduced acromiohumeral space
RA in hips and knees
uniform loss in all joint spaces, joint deformities, subchondral cysts, baker’s cysts
RA in spine
50% of patients with RA will have cervical spine involvement, causing erosions within facet capsules around ligament and tendon attachments
management for RA
RA factor + (most of the time)
anti-CCP antibodies present
ESR and CRP elevated
-ANA
radiographic re-evaluation every 6-12 months until stable; MRI for panus and neuro effects
don’t adjust fused or hypermobile segments
recommend adequate sleep, dietary changes, exercise
refer to rheumatologist for pharmacology (NSAID, corticosteroids, anti-rheumatic drugs)
SLE demographics
30-50yo females
blacks slightly higher than whites
clinical findings of SLE
malar rash
joint deformities
serious multisystem disease of kidneys, liver, lymphatics, joints
scleroderma demographics
30-60 yo woman
blacks more than whites
serious multi-system disease of connective tissue
may have CREST (calcinosis, raynaud’s, esophageal lesions, sclerodactyly, telangiectasia
scleroderma in hands
ungual tuft resorption/acral osteolysis/distal tuft resorption
soft tissue atrophy, soft tissue calcification, erosions in the DIPs, PIPs, and MCPs
calcifications are distinctive (dense, globular, clumpy)
scleroderma management
chest films
chest CT
upper GI contrast studies
refer to rheumatologist
seronegative spondyloarthropathies
AS
enteropathic
psoriasis
reactive
most seronegative spondyloarthropathies have what lab finding?
HLA-B27 (present in most to varying degrees)
ESR, CRP elevated
ANA -
Marie-Strumpell demographics
AS
most common inflammtory spondyloarthropathy, onset around late 20s and early 30s
males more than females
AS in the spine and pelvis
SI is typically the first and most common site of involvement (50% will have full SI ankylosis)
squaring of vertebrae, syndesmophytes (marginal, thin, gracile), romanus lesion, shiny corner sign, dagger sign, railroad sign, trolly track sign
AS management
plain films
MRI and CT to further define osseous changes and characterize any neurological complications
HLA-B27, ESR+, RA-, ANA-
educate on safe activities
joint mobilization, posture and thoracic expansion exercises
allopaths (anti-inflammatories, rheumoatologist
enteropathic arthritis
causes
chron’s disease, ulcerative colitis, whipple disease, GI infections, cirrhosis
enteropathic arthritis
what spine looks like on xray
squaring of the vertebrae syndesmophytes romanus lesion shiny lesion shiny corner sign dagger sign railroad sign trolley track sign
managment for enteropathic arthritis
almost same as AS, but HLA B27 in 60-70%, ESR up, RA and ANA -
refer to gastroenterologist, internist, rheumatologist
psoriatic arthritis description
most people with dermatological psoriasis DON’T have inflammatory arthritis
rarely would someone have arthritis and not skin lesions
usually occurs around 30-50yo
equal occurance in females and males
how is PA similar to AS and RA? different?
similar: erosions, symmetrical joint space narrowing, eventual ankylosis
different: asymmetrical distribution about body and digit, normal bone density, peri-ostitis, acro-osteolysis
PA in extremities
sausage digit ray pattern mouse ears pencil in cup osteolysis
PA in spine and pelvis
SI erosions and eventual ankylosis
spine findings are key in distinguishing features of PA vs other causes of sacroiliitis
PA managment
evaluate skin and nails for lesions
serological studies (HLA B27 up, RA and ANA -
chiro care: be wary of hypermobility and ankylosis
allopath: NSAIDs, anti-rheumatic drugs, refer to rheumatologist
reactive arthritis
non-marginal, thick, bulky, may be discontiguous not common males (adolescent-mid 30s usually follows gastrointestinal or genitourinary infection may also be linked to genetic factors iritis urethritis athritis
reactive arthritis treatment
treat infection first, then spondyloarthropathy may resolve
metabolic and crystal-induced arthropathies
gout
CPPD
ochronosis
gout
MC inflammatory arthritis in men older than 40
40-50 yo men
too much uric acid in blood (produce too much or can’t clear enough)
most patients with gout don’t develop tophacious gout
crystals accumulate in and around joints, leading to erosions with “overhang”, lump and bumpy digits
gout managment
plain films won’t show tophi until years after the disease
labs (hyperuricemia)
lifestyle modifications- evaluation of triggers that lead to the attack
allopath: anti-inflammatory medications, xanthene oxidase inhibitors
chondrocalcinosis
CPPD
middle-aged and older
equal among males and females
associated with hyperparathyroidism, diabetes, hemochromatosis, gout, neuropathic arthropathies (syphilis, diabetes)
chondrocalcinosis management
gold standard is joint aspiration to look for crystals
chiro care: exercise, joint mobilization
allopath: NSAIDs
calcific tendonitis
HADD
not a crystal induced arthropathy, but can get mixed up with CPPD
typically monoarticular and MC in shoulder as dense calcification
calcific tendonitis management
HADD
degenerative, treated as OA; some modalities may lessen symptoms (laser, US)
septic arthritis
infections do not respect anatomical boundaries (they’ll destroy all tissues)
discs: rapid loss of disc height and development of endplate erosions
joints: rapid loss of joint space and development of cortical erosions
septic arthritis management
CT for cortical destruction, MRI for marrow destruction, refer to ortho for aspiration, antibiotics, curretage, management of risk factors (HIV, diabetes, UTI)
