Orthopedics/Musculoskeletal Flashcards

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1
Q

What percentage of back pain resolves on its own?

A

90% resolve in 6 weeks, <5% become chronic

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2
Q

What is the pathophysiology of a pinched nerve (radiculopathy)?

A

When the inner core (nucleus pulposus) of the intervertebral disc bulges out through the outer layer of ligaments that surround the disc (annulus fibrosis). This tear in the annulus fibrosis causes pain in the back at the point of herniation. If the protruding disc presses on a spinal nerve, the pain may spread to the area of the body that is served by that nerve.

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3
Q

What are the stages of nuclear herniation?

A

Nuclear herniation, disc protrusion, nuclear extrusion and nuclear sequestration

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4
Q

What is the etiology of back pain?

A

Mechanical (98%):
- Sprain (ligament), strain (muscle), facet joint degeneration (OA), disc degeneration/herniation, spinal stenosis (e.g. spondylosis), spondylolisthesis, compression fracture

Non-Mechanical (2%):

  • Surgical Emergencies: cauda equina syndrome), AAA (pulsatile abdominal mass)
  • Medical Conditions:
  • Neoplastic (primary, metastatic, multiple myeloma)
  • Infectious (osteomyelitis, TB)
  • Metabolic (osteoporosis, osteomalacia, Paget’s disease)
  • Rheumatologic (ankylosing spondylitis, polymyalgia rheumatica)
  • Referred pain (perforated ulcer, pancreatitis, pyelonephritis, ectopic pregnancy, herpes zoster)
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5
Q

What time period is acute back pain?

A

Acute: <4wks

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6
Q

What time period is sub-acute back pain?

A

Subacute: 4-12wks

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7
Q

What time period is chronic back pain?

A

Chronic: >12 wks

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8
Q

Herniated disc is unlikely in a _____ as the nucleus pulposus is already _____, thus commoner in younger people. Older people can still have pinched nerves but different process - smaller joint spaces

A

50+ yo

Fibrotic

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9
Q

When discs protrude at a level, they often compress the spinal nerve root (has dorsal and ventral root) of the segment _____!

A

Below

For instance if you have an L4/L5 nerve root disc herniation, you can affect the L4 root which is in that area, but often affects the L5 one. Why? The intervertebral foramina are pretty big in the lumbar region (small in the cervical region). But the nerve root is up really high in the foramen, above the disc. If the disc pushes out, it is likely to spare the nerve root because the root will be above, but instead it will push against the level below

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10
Q

What are the red flags of acute lower back pain?

A

B: owel or bladder dysfunction; sudden onset (Emergency, refer w/n hours)

A: nestheia (saddle) (Emergency, refer w/n hours)

C: onstitutional symptoms, weight loss, hx of cancer, fever (Urgent, refer w/n 24-48 hours)

K-(C): hronic disease, severe, constant or worsening pain (PM or supine) (Urgent, refer w/n 24-48 hours)

P: aresthesia (Urgent, refer w/n 24-48 hours)

A: ge > 50 (Soon, refer w/n weeks) + mild trauma (Urgent, refer w/n 24-48 hours)

I: V drug use/infection (Urgent, refer w/n 24-48 hours)

N: euromotor deficits (Urgent, refer w/n 24-48 hours)

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11
Q

What are the yellow flags of acute lower back pain?

A

Belief that pain and activity are harmful, sickness behaviours (extended rest), low/negative mood, social withdrawal, treatment expectations that do not fit best practice, problems with claim/compensation, history of back pain/time-off/other claims, problems at work, poor job satisfaction, heavy work, unsociable hours (shift work), overprotective family or lack of support

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12
Q

Clinical features of cauda equina syndrome and features on physical exam?

A

Pain is usually the first symptom of cord compression, but motor (lower extremity weakness, areflexia, decreased anal tone) and sensory findings (saddle anesthesia). Fecal incontinence, urinary retention are often late findings

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13
Q

Clinical features of infectious back pain and features on physical exam?

A

Long use of corticosteroids; Unexplained fever, malaise; IV drug use, Recent spinal injection or epidural catheter placement. The pain is not relieved with rest and is provoked by weight bearing. On examination there will be focal tenderness at the involved spinous process.

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14
Q

Clinical features of cancer for back pain and features on physical exam?

A

Hx of Ca + new back pain; Unexplained weight loss; Duration > 6wks; Age >70. Focal tenderness at the involved vertebrae

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15
Q

In patients with a history of cancer, sudden, severe pain raises concern for ______?

A

Pathologic fracture.

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16
Q

What is pinched nerve (radiculopathy)?

A

Pressure or impingement on nerve roots in spinal canal

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17
Q

Clinical features of vertebral compression fracture and features on physical exam?

A

Acute onset of localized back pain which may be incapacitating - worse with flexion and often point tenderness on palpation. There may be no history of preceding trauma

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18
Q

What is sciatica?

A

Sciatica is a nonspecific term used to describe a variety of leg or back symptoms. Usually, sciatica refers to a sharp or burning pain radiating down from the buttock along the course of the sciatic nerve (the posterior or lateral aspect of the leg, usually to the foot or ankle).

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19
Q

What are the causes of spinal stenosis?

A

Spondylosis (degenerative arthritis affecting the spine), spondylolistheses (slipping of a vertebra in relation to the one below), and thickening of the ligamentum flavum

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20
Q

What is spinal stenosis?

A

Narrowing of the spinal canal by a piece of bone

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21
Q

Over 90 percent are ______ radiculopathies.

A

Over 90 percent are L5 and S1 radiculopathies

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22
Q

Risk factors for osteoporotic fracture include _____ and _____.

A

Advanced age and chronic glucocorticoid use

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23
Q

What are the causes of pinched nerve (radiculopathy)?

A

Causes: herniated disc, degenerative disc disease, bone spurs/osteophytes, spinal stenosis.

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24
Q

_____ is a hallmark of lumbar spinal stenosis

A

Neurogenic claudication

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25
Q

What are the symptoms of spinal stenosis?

A

Ambulation-induced (walking, standing or extension) pain localized to the calf and distal lower extremity resolving with sitting or leaning forward

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26
Q

Clinical features of ankylosing spondylitis and associated features?

A

Morning stiffness; Improves with exercise; Younger age males, pain at night. Associated with uveitis and colitis

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27
Q

Clinical features of lumbosacral muscle strains/sprains and features on physical exam?

A

Often following isolated traumatic incidents or repetitive overuse; pain worse with movement, relieved by rest; examination may reveal restricted range of motion, muscle tenderness, or trigger points

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28
Q

Clinical features of lumbar spondylosis?

A

More common in persons older than 40 years; pain may be present in or radiate from the hips; pain is worse with activity; pain may worsen with lumbar spine extension or rotation

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29
Q

Clinical features of osteoarthritis and in which age group does it commonly present in?

A

Low back pain may be a symptom of osteoarthritis of the facet joints spine. Patients may also complain of hip pain, either from osteoarthritis of the hip or referred pain from the spine. Osteoarthritis most commonly presents in patients over the age of 40. Pain is typically exacerbated by activity and relieved by rest

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30
Q

______ may contribute to the severity symptoms of low back pain or may be a cause of nonorganic back pain

A

Psychologic distress (eg, depression or somatization)

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31
Q

What is spondylolysis and activities that can cause it?

A

Break in the pars interarticularis, (scotty dog has a ring around his neck), typically stress fracture, pain with activities involving lumbar extension - weightlifting, gymnastics. Pain in young adolescent athletes

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32
Q

What should be asked on history for back pain?

A

o OPQRST
o Back/Buttock dominant vs leg dominant
o Constant vs intermittent pain
o What increases your typical pain?
▪ Flexion (possibly extension) – disc pain
▪ Extension only – facet joint pain
▪ All movements (improved with rest) – compressed nerve pain
▪ Walking or standing (relieved with sitting or flexion) – spinal stenosis
o Red Flags – bowel or bladder incontinence
o Medications

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33
Q

Indications for Lumbar Xray

A
▪	No improvement after 6 wk
▪	Fever >38oC
▪	Unexplained weight loss
▪	Prolonged corticosteroid use
▪	Significant trauma
▪	Progressive neurological deficit
▪	Suspicion of ankylosing spondylitis
▪	History of cancer (rule out metastases)
▪	Alcohol/drug abuse (increased risk of osteomyelitis, trauma, fracture)
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34
Q

Work up for back pain?

A

Work-Up: plain films not recommended in initial evaluation
o If Infection/Cancer Suspected: CBC, CRP
o If Neuro Deficits Worsening or Infection/Cancer Suspected: consider CT or MRI

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35
Q

What are the special tests that can be done for back pain?

A
▪	Straight leg raise
▪	Crossed straight leg raise 
▪	Femoral stretch test 
▪	FABER 
▪	Thomas
▪	Romberg
▪	Schober
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36
Q

What are the symptoms of benign back pain?

A

Benign Back Pain: moderate, dull, aching, worse with movement or cough

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37
Q

What vascular emergencies should you rule out for acute back pain?

A

Aortic dissection, AAA, PE, MI, retroperitoneal bleed

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38
Q

What are the causes of spinal emergencies?

A

Osteomyelitis, cauda equina, epidural abscess or hematoma

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39
Q

How do you evaluate risk for fracture/infection/cancer/vascular causes of acute back pain?

A

Osteoporosis, age, IV drug user, recent spinal intervention, immunosuppression, cardiac risk factors

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40
Q

What are the physical exam

A

o Inspection: curvature, posture, gait
o Palpation: bony deformities/spine for bony tenderness, paraspinal muscle bulk/tenderness, trigger points
o Percussion: of spine to elicit pain due to fracture or infection
o Move: ROM and peripheral pulses
o Neuro Exam: for L4/L5/S1 helps determine level of spinal involvement (power, reflexes, sensation)
o Other Exam: precordial, respiratory, abdominal and neurological exams guided by history
o Special Tests

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41
Q

What is straight leg raise and what does it help diagnose?

A

Straight leg raise (positive if pain at <70 degrees and aggravated by ankle dorsiflexion) = (+)Sciatica

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42
Q

What is the femoral stretch test and what does it help diagnose?

A

Femoral stretch test (patient prone, knee flexed, examiner extends hip) to diagnose L4 radiculopathy

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43
Q

What is FABER and what does it help diagnose?

A

FABER (Flex, abduct, externally rotate knee)

SI joint pain– osteoarthritis

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44
Q

What is crossed straight leg raise?

A

Crossed straight leg raise (raising of uninvolved leg elicits pain in leg with sciatica), more specific than straight leg raise

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45
Q

What is the Thomas test and what does it help diagnose?

A

Hand under lumbar spine, flex opposite knee, observe angle between femur and table

Angle >0 – Flexed hip contracture

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46
Q

What is the Romberg test and what does it help diagnose?

A

Patient stands feet together, arms outstretched at 90, eyes closed

Loss of balance - Pathology of dorsal columns or vestibular system

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47
Q

What is the Schober test and what does it help diagnose?

A

Mark 5cm below and 10cm above L5, patient bends forward, measure distance between marks

Distance increase <5cm - Muscle tightness, ankolyosing spondyitis, scoliosis

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48
Q

Management of chronic back pain (>12wks since onset)?

A

▪ Rx: physical or therapeutic exercise
▪ Analgesics: acetaminophen, NSAIDs (consider PPI), low dose TCAs (amitriptyline), short term cyclobenzaprine PRN
▪ Referral Options: community based rehab or self-management/CBT
▪ Additional Options: progressive muscle relaxation, acupuncture, massage, TENS, aqua therapy, yoga

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49
Q

Management of moderate to severe chronic back pain (>12wks since onset)?

A

Opioids, multidisciplinary chronic pain program, epidural steroids (short term relief of radicular pain), prolotherapy, facet joint injections, surgery(?)

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50
Q

Management of spinal infection?

A

Early IV antibiotics and ID consultation

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51
Q

Management of lumbosacral strain + disc herniation?

A

Analgesia and continue daily activities as much as tolerated; discuss red flags and organize follow-up
▪ Discectomy (removal of part of disc that is compressing nerve)
▪ Disc prosthesis occasionally used (newer procedure, beneficial in younger more active patients)
▪ Epidural Injection

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52
Q

Management of cauda equine syndrome?

A

Dexamethasone + lumbosacral MRI + early neurosurgical consultation

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53
Q

Management of acute back pain (<12wks since onset)?

A

▪ Education: low back pain typically resolves within a few weeks (70% in 2 weeks, 90% in 6 weeks)
▪ Rx: alternating cold and heat, continue activities as tolerated; encourage early return to work, physical activity and/or exercise
▪ Analgesics: acetaminophen > NSAIDS, short course muscle relaxants, short-acting opioids (rarely), spinal traction
▪ Follow-up in 1-6 weeks
▪ Consider Referral: physical therapist, chiropractor, physiatrist, spinal surgeon (if unresolving radicular symptoms), multidisciplinary pain program (if not returning to work)

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54
Q

Definition of monoarthritis?

A

1 joint involved

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55
Q

Definition of oligoarthritis?

A

2-4 joints involved

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56
Q

Definition of polyarthritis?

A

> 5 joints involved

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57
Q

The spondyloarthropathies are classically ____, whereas rheumatoid arthritis (RA) is usually ____.

A

Oligoarticular

Polyarticular

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58
Q

Polyarticular/Oligoarticular DDx

A
  1. Mechanical: OA
  2. Inflammatory
  3. Infections
  4. Endocrine/metabolic: hypo/hyperthyroidism, hyperparathyroidism, hemochromatosis, Wilson’s disease
  5. Malignancies: acute leukemia
  6. Sarcoidosis: lofgren’s syndrome
  7. Familial mediterranean fever
  8. Polymyalgia rheumatica
  9. Mucocutaneous disorders: dermatomyositis, erythema nodosum, erythema multiforme, pyo derma gangrenosum, pustular psoriasis
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59
Q

Inflammatory etiology of polyarticular/oligoarticular disease?

A
  • Rheumatoid arthritis
  • Spondyloarthropathies - psoriatic arthritis, enteric arthritis, reactive arthritis, AS
  • Crystal induced: gout, pseudogout
  • Connective tissue diseases – SLE, Sjogrens, myositis
  • Vasculitis: polymyalgia rheumatica, wegener’s Granulomatosis, behcet’s disease, still’s disease
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60
Q

Infectious etiology of polyarticular/oligoarticular disease?

A
  • Bacterial: septic (gonococci) – usually monoarticular, meningococci, endocarditis, lyme disease, whipple’s disease, mycobacteria
  • Viral: parvovirus, rubella, hbv, hcv, hiv, ebv
  • Fungal
  • Post-infectious/reactive: enteric infections, genitourinary infections, rheumatic fever, inflammatory bowel disease
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61
Q

Red flags for polyarticular/oligoarticular disease?

A

Abnormal vitals, symptoms > 6 weeks, immunocompromised, rapid onset/progression, STI/IVDU, non-weight bearing, constitutional symptoms

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62
Q

Questions asked on HPI for polyarticular/oligoarticular disease?

A

HPI:

  • Timing of onset (acute vs chronic) – symmetric vs asymmetric
  • Jt swelling, jt pain, decreased ROM
  • Hx of joint trauma
  • Identify involved joints
  • Features of RA or OA
  • Reactive arthritis symptoms - rash, conjunctivitis, urethritis/cervicitis
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63
Q

Lofgren syndrome triad?

A

Triad: bilateral ankle swelling, erythema nodosum, hilar lymphadenopathy

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64
Q

Possible skin and nails findings on physical exam for polyarticular/oligoarticular disease?

A
  • Rashes: pustular lesions (disseminated gonococcal infection), erythema migrans (Lyme), erythema nodosum (IBD, sarcoidosis), psoriasis/nail pitting/onycholysis
  • Tophi (gout)
  • Lesions on glans penis (reactive arthritis)
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65
Q

Investigations for polyarticular/oligoarticular disease?

A
  1. Labs
    - CBCd – may have anemia of chronic disease, leukocytosis/leukopenia, thrombocytosis/thrombocytopenia
    - Electrolytes, Cr, CRP* (main one), liver enzymes, urinalysis, serum urate
    - If Suspected RA: RF (>20), anti-CCP
    - If suspected connective tissue disorder: ANA, anti-dsDNA, C3/C4, urine protein-Cr ratio, CK
    - If suspected seronegative spondyloarthropathy: HLA-B27
    - If suspected vasculitis: ANCA, anti-GBM
  2. Arthrocentesis
  3. Xray
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66
Q

What should you send the synovial fluid for in an arthrocentesis

A

Complete cell count + differential, gram stain, culture, crystals (gold standard)

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67
Q

Synovial fluid findings for OA?

A
  • Cell count = 200-2000
  • Polys = <25%
  • Crystals = occasional CPPD (calcium pyrophosphate disease) - Pseudogout, can calcify cartilage
    be aging
  • Gm stain and culture = negative
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68
Q

Synovial fluid findings for inflammatory arthritis?

A
  • Cell count = 2,000-50,000
  • Polys = >50%
  • Crystals = none
  • Gm stain and culture = negative
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69
Q

Synovial fluid findings for septic arthritis?

A
  • Cell count = >50,000
  • Polys = >75%
  • Crystals = none
  • Gm stain and culture = positive
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70
Q

Inflammatory arthritis symptoms?

A
  • Pain at rest, relieved by gentle motion
  • Morning stiffness >1 h
  • Warmth, swelling, erythema
  • Malalignment/deformity (late finding)
  • Extra-articular manifestations
  • Nighttime awakening due to pain
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71
Q

Degenerative arthritis symptoms?

A
  • Pain with motion, relieved by rest
  • Morning stiffness <1/2 h
  • Joint instability, buckling, locking
  • Bony enlargement, malalignment/deformity (late finding)
  • Evening/end of day pain
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72
Q

Seronegative spondyloarthropathies Ddx?

A
  • Psoriatic arthritis
  • Enteric arthritis
  • Ankylosing spondylitis
  • Reactive arthritis
  • Undifferentiated
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73
Q

Clinical features of seronegative spondyloarthropathies

A
  • SPONDYLOARTHROPATHY spondylitis, sacroiliitis, morning stiffness >30 min
  • OLIGOARTHRITIS asymmetric, dactylitis, usually larger joints, lower extremities (exception: PsA)
  • ENTHESOPATHY inflammation at the sites of insertion of ligaments, tendons, joint capsule, and fascia to bone, with both destruction and new bone formation. This results in Achilles tendonitis, plantar fasciitis, tenosynovitis, and dactylitis/sausage fingers
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74
Q

Extraarticular changes of seronegative spondyloarthropathies

A

Nail pitting, onycholysis, psoriasis, tenosynovitis, dactylitis, synovitis, acute uveitis, aortic regurgitation, apical pulmonary fibrosis, chin to chest distance, occiput to wall distance, decreased chest expansion, cauda equine compression, and enthesitis (costochondritis, patellar and Achilles tendonitis, plantar fasciitis).

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75
Q

Serology HLA B27 ____, rheumatoid factor ____ (hence, why they are called seronegative spondyloarthropathies).

A

Positive

Negative

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76
Q

Back exam for seronegative spondyloarthropathies?

A
  • INSPECTION swelling, erythema, atrophy, scars, and loss of thoracic kyphosis and cervical/lumbar lordosis
  • RANGE OF MOTION check gait and flexion, extension, lateral bending, rotation
  • PALPATION tenderness over spinous processes and sacroiliac joints
  • SPECIAL TESTS Schober’s test (place mark 5 cm below and mark 10 cm above the spine at level of PSIS/L5 with patient standing. A distance increase of <5 cm [<2 in.] between the marks with the patient bending forward suggests limited lumbar flexion), finger to floor distance, occiput to wall distance. Perform FABER test (SI joint stability) and straight leg raising test (sciatica)
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77
Q

Clinical features/physical exam findings of ankylosing spondylitis?

A
  • Spondylitis, sacroiliitis, morning stiffness, and arthritis of the hips, knees, shoulders, and occasionally peripheral joints.
  • Loss of lumbar lordosis and thoracic kyphosis with significant decreased range of motion and chest expansion
  • Positive Schober’s test and occiput to wall test.
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78
Q

Extraarticular manifestations of ankylosing spondylitis?

A

Extraarticular manifestations include anterior uveitis, C1-2 subluxation, restrictive lung disease, aortic regurgitation, conduction abnormalities, and secondary amyloidosis.

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79
Q

Imaging findings of ankylosing spondylitis?

A

Imaging reveals bamboo spine (syndesmophytes), shiny corners (squaring and increased density anteriorly of vertebral bodies), and whiskering (new bone and osteitis at tendon and ligament insertions)
• Large joints: synovitis indistinguishable from RA
• Spine: enthesitis: inflammation visualized as bone marrow edema at entry of ligaments into bone. (not synovitis here)

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80
Q

New York diagnostic criteria for ankylosing spondylitis?

A
  • CLINICAL CRITERIA low back pain and morning stiffness of >3 months, limitation of motion of the lumbar spine in both the sagittal and frontal planes, and limitation of chest expansion (<2.5 cm [1 in.])
  • RADIOLOGIC CRITERIA sacroiliitis with more than minimum abnormality bilaterally or unequivocal abnormality unilaterally
  • DIAGNOSIS one clinical plus one radiologic criterion = definite AS; three clinical criteria or one radiologic criterion only = probable AS
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81
Q

Treatment of ankylosing spondylitis?

A

Aggressive NSAID (indomethacin) and exercise, TNF-inhibitors

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82
Q

Clinical features of reactive arthritis?

A
  • <5 joints involved, proximal and distal, asymmetric, other systems include urethritis, dysentery, skin, eye
  • Spondylitis, sacroiliitis, morning stiffness, lower limb arthritis (asymmetric oligoarthritis of lower limbs), and enthesitis (Achilles tendonitis, plantar fasciitis, chest wall changes, and sausage fingers/toes).
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83
Q

Pathophysiology of reactive arthritis?

A

Preceding/ongoing infectious disorders such as urethritis (Chlamydia), diarrhea (Shigella, Salmonella, Campylobacter, Yersinia) or HIV, usually within 6 weeks.

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84
Q

Physical exam findings of reactive arthritis?

A
  • Genital lesions (circinate balanitis with shallow painless ulcers on the glans or urethral meatus, urethritis, prostatitis)
  • Skin lesions (keratoderma blennorrhagica with vesicles that progress to macules, papules and nodules on palms and soles)
  • Eye lesions (conjunctivitis, iritis [acute, unilateral, photophobia, pain, redness, impaired vision])
  • Bowel inflammation (acute enterocolitis, chronic ileocolitis)
  • Cardiac abnormalities (aortic regurgitation, conduction abnormalities).
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85
Q

Imaging findings of reactive arthritis?

A

Plain film reveals fluffy erosions, periosteal spurs, and asymmetric syndesmophytes

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86
Q

Reactive arthritis triad?

A
  • “can’t see, can’t pee, can’t climb a tree”–> conjunctivitis, urethritis/cervicitis, arthritis
  • Urethritis (chlamydia) or dysentery (SEXCY) followed by arthritis, conjunctivitis, painless oral ulcers and typical skin lesions (balanitis, keratoderma)
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87
Q

Treatment of reactive arthritis?

A

NSAIDs, sulfasalazine, anti-TNF agents, methotrexate, azathioprine, leflunomide

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88
Q

Ddx for musculoskeletal lump/mass?

A
  1. Soft tissue
    - Benign (e.g., lipoma)
    - Malignant (e.g., leiomyosarcoma)
  2. Bone (e.g., cyst)
    - Benign (e.g., cyst)
    - Malignant (e.g., Ewing sarcoma)
  3. Non-neoplastic
    - Infectious (e.g., osteomyelitis)
    - Traumatic (e.g., hematoma)
    - Inflammatory (e.g., rheumatoid nodules, tendonitis)
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89
Q

What should be asked on history for musculoskeletal lump/mass?

A
  • Lump: Onset, recent changes (size, colour, rapid growth), provoking factors, trauma (hematoma), cut (abscess), warmth, pain
  • Systemic: fever, night sweats, weight loss, fatigue
  • PMHx: previous malignancy, illnesses
  • FHx: cancers in family
  • Meds:
  • Social: smoking, alcohol intake
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90
Q

Physical exam for musculoskeletal lump/mass?

A
  • Inspection: location, appearance, SEADS
  • Palpation: temp, tenderness, consistency (soft, rubbery, firm, stony hard, or nodular, lobulated), contour (irregular), surface (smooth, rough, irregular), depth, size, pulsation
  • Tethered to skin (mobile or fixed), muscle or tendon involvement
  • Special tests: transilluminability - should be done in a darkened room, with pen torch directly on lump. Fluid-filled lumps like cysts or hydrocele are transilluminable, while solid lumps are not.
  • Regional LN exam, neuro exam
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91
Q

What should you comment on an Xray of a musculoskeletal lump/mass?

A
  • Internal calcification may be signs of a vascular tumour, heterotopic ossification, or rare forms of sarcoma.
  • Advanced imaging including MRI may demonstrate signs of malignancy or aggressive masses.
  • Large size (>5cm).
  • Deep.
  • Heterogeneous.
  • Incorporating the neurovascular bundle.
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92
Q

Treatment of musculoskeletal lump/mass?

A
  • Infection should be treated with irrigation & debridement and antibiotics
  • Most benign masses may be excised in symptomatic
  • Most malignant masses benefit from radiation treatment followed by wide resection
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93
Q

What is a lipoma?

A

Single or multiple non-tender subcutaneous tumours that are soft and mobile

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94
Q

_____ tumours to bone are much more common than primary bone tumours, particularly if age >40 yr

A

Metastatic

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95
Q

Pathophysiology of a lipoma?

A

Adipocytes enclosed in a fibrous capsule

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96
Q

Investigations for a lipoma?

A

Biopsy only if atypical features (painful, rapid growth, firm)

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97
Q

Management of a lipoma?

A

Reassurance, excision or liposuction only if desired for cosmetic purposes

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98
Q

Clinical features of bone tumors?

A
  • Malignant (primary or metastasis): local pain and swelling (weeks to months), worse on exertion and at night, soft tissue mass
  • Benign: usually asymptomatic
  • Minor trauma often initiating event that calls attention to lesion
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99
Q

Xray findings of bone tumors?

A
  • Lytic, lucent, sclerotic bone
  • Involvement of cortex, medulla, soft tissue
  • Radiolucent, radiopaque, or calcified matrix
  • Periosteal reaction
  • Permeative margins
  • Pathological fracture
  • Soft tissue swelling
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100
Q

Red flags of bone tumors?

A
  • Persistent skeletal pain
  • Localized tenderness
  • Spontaneous fracture
  • Enlarging mass/soft tissue swelling
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101
Q

Ddx of benign active bone tumors?

A
  1. Bone-Forming Tumors
    - Osteoid Osteoma
  2. Fibrous Lesions
    - Fibrous Cortical Defect
    - Osteochondroma
    - Enchondroma
  3. Cystic Lesions
    - Unicameral/Solitary Bone Cyst
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102
Q

What is an osteoid osteoma?

A

Bone tumour arising from osteoblasts

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103
Q

When and where do osteoid osteoma typically occur?

A
  • Peak incidence in 2nd and 3rd decades, M:F=2:1
  • Proximal femur and tibia diaphysis most common locations
  • Not known to metastasize
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104
Q

Radiographic findings of osteoid osteoma?

A

Small, round radiolucent nidus (<1.5cm) surrounded by dense sclerotic bone (“bull’s-eye”)

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105
Q

Symptoms of osteoid osteoma?

A

Produces severe intermittent pain from prostaglandin secretion and COX1/2 expression, mostly at night (diurnal prostaglandin production), thus is characteristically relieved by NSAIDs

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106
Q

Treatment of osteoid osteoma?

A

NSAIDs for night pain; surgical resection of nidus; ablation of the small radiolucent zone with percutaneous radiofrequency energy

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107
Q

Most common benign bone tumour in children, typically asymptomatic and an incidental finding

A

Fibrous Cortical Defect i.e.non-ossifying fibroma, fibrous bone lesion

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108
Q

What are fibrous cortical defects?

A

These lesions are developmental defects in which parts of bone that normally ossify are instead filled with fibrous tissue

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109
Q

Location of fibrous cortical defects?

A

Femur and proximal tibia most common locations, 50% of patients have multiple defects that are usually bilateral, symmetrical, metaphysis

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110
Q

Radiographic findings of fibrous cortical defects?

A

Diagnostic, radiolucent metaphyseal eccentric ‘bubbly’ lytic lesion near physis; thin, smooth/lobulated, well-defined sclerotic margin

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111
Q

Treatment of fibrous cortical defects?

A

Most lesions resolve spontaneously

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112
Q

What is an osteochondroma?

A
  • Cartilage capped bony tumour

- Most common of all benign bone tumours: 45%

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113
Q

What are the two types of osteochondroma?

A

Sessile (broad based and increased risk of malignant degeneration) vs. pedunculated (narrow stalk)

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114
Q

Location of osteochondroma?

A

Metaphysis of long bone near tendon attachment sites (usually distal femur, proximal tibia, or proximal humerus)

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115
Q

Radiographic findings of osteochondroma?

A

Cartilage-capped bony spur on surface of bone (“mushroom” on x-ray)

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116
Q

Treatment of osteochondroma?

A

Typically observation; surgical excision if symptomatic (compressing nerve/vessel)

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117
Q

What is an enchondroma?

A

Benign cartilaginous growth, an abnormality of chondroblasts, develops in medullary cavity

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118
Q

Where do enchondromas occur?

A

60% occur in the small tubular bones of the hand and foot; others in femur, humerus, ribs

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119
Q

Pain in absence of pathologic fracture is an important clue for malignant degeneration to _____ for suspected enchondroma?

A

Chondrosarcoma

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120
Q

Radiographic finding of enchondromas?

A
  • Single/multiple enlarged rarefied areas in tubular bones

- Lytic lesion with sharp margination and irregular central calcification (stippled/punctate/popcorn appearance)

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121
Q

Treatment of enchondromas?

A

Observation with serial x-rays; surgical curettage if symptomatic or lesion grows

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122
Q

Most common cystic lesion; serous fluid-filled lesion

A

Unicameral/Solitary Bone Cyst

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123
Q

In unicameral/solitary bone cyst the cortex thins and predisposes the area to a ____

A

Buckle-like pathologic fracture

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124
Q

Most common location of unicameral/solitary bone cyst

A

Proximal humerus and femur most common

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125
Q

Symptoms of unicameral/solitary bone cyst

A

Asymptomatic, or local pain; complete pathological fracture (50% of presentations) or incidental detection

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126
Q

Radiographic findings of unicameral/solitary bone cyst

A

Lytic translucent area on metaphyseal side of growth plate, cortex thinned/expanded; well-defined lesion

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127
Q

Treatment of unicameral/solitary bone cyst?

A

Aspiration followed by steroid injection; curettage ¬ ± bone graft indicated if re-fracture likely

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128
Q

When do giant cell tumours/aneurysmal bone cyst/osteoblastomas occur?

A

Affects patients of skeletal maturity, peak 3rd decade

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129
Q

Location of osteoblastoma?

A

Found in the distal femur, proximal tibia, distal radius, sacrum, tarsal bones, spine

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130
Q

Radiographic findings of giant cell tumors?

A

Eccentric lytic lesions in epiphyses adjacent to subchondral bone; may break through cortex; T2 MRI enhances fluid within lesion (hyper-intense signal)

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131
Q

Radiographic findings of aneurysmal bone cyst?

A
  • Either solid with fibrous/granular tissue, or blood-filled
  • Expanded with honeycomb shape
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132
Q

Symptoms of giant cell tumours/aneurysmal bone cyst/osteoblastomas?

A

Local tenderness and swelling, pain may be progressive (giant cell tumours), ± symptoms of nerve root compression (osteoblastoma)

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133
Q

Treatment of giant cell tumours/aneurysmal bone cyst/osteoblastomas?

A
  • Intralesional curettage + bone graft or cement

- Wide local excision of expendable bones

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134
Q

Radiographic findings of osteoblastoma

A

Often nonspecific; calcified central nidus (>2 cm) with radiolucent halo and sclerosis

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135
Q

Ddx of malignant bone tumors?

A
  • Osteosarcoma
  • Chondrosarcoma
  • Ewing’s Sarcoma
  • Multiple Myeloma
  • Metastatic bone cancer
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136
Q

Most frequently diagnosed in 2nd decade of life (60%), 2nd most common primary malignancy in adults

A

Osteosarcoma

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137
Q

Ask about history of what if suspecting osteosarcoma?

A

History of Paget’s disease (elderly patients), previous radiation treatment

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138
Q

Location for osteosarcoma

A

Predilection for sites of rapid growth: distal femur (45%), proximal tibia (20%), and proximal humerus (15%)

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139
Q

Radiographic findings of osteosarcoma

A
  • characteristic periosteal reaction: Codman’s triangle or “sunburst” spicule formation (tumour extension into periosteum)
  • destructive lesion in metaphysis may cross epiphyseal plate
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140
Q

Management of osteosarcoma?

A

Complete resection (limb salvage, rarely amputation), neo-adjuvant chemo; bone scan- rule out skeletal metastases, CT chest - rule out pulmonary metastases

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141
Q

Symptoms of osteosarcoma

A

Painful symptoms: progressive pain, night pain, poorly defined swelling, decreased ROM

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142
Q

What is primary chondrosarcoma?

A

Primary (2/3 cases): previous normal bone, patient >40 yr; expands into cortex to cause pain, pathological fracture

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143
Q

What is secondary chondrosarcoma?

A

Malignant degeneration of pre-existing cartilage tumour such as enchondroma or osteochondroma. Age range 25-45 yr, better prognosis than primary chondrosarcoma

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144
Q

Symptoms of chondrosarcoma?

A

Progressive pain, uncommonly palpable mass

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145
Q

Radiographic findings of chondrosarcoma?

A

In medullary cavity, irregular “popcorn” calcification

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146
Q

Treatment of chondrosarcoma?

A

Unresponsive to chemotherapy, treat with aggressive surgical resection + reconstruction; regular follow-up X-rays of resection site and chest

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147
Q

What is Ewing’s sarcoma?

A
  • Malignant, small round cell sarcoma

- Most occur between 5-25 yr old

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148
Q

Radiographic findings of Ewing’s sarcoma?

A

Presents with pain, mild fever, erythema, and swelling; anemia, increased WBC, ESR, LDH (mimics an infection)

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149
Q

Signs/symptoms of Ewing’s sarcoma?

A

Moth-eaten appearance with periosteal lamellated pattern (“onion-skinning”) in metaphyses of long bone with diaphyseal extension

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150
Q

Treatment of Ewing’s sarcoma?

A

Resection, chemotherapy, radiation

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151
Q

What is multiple myeloma?

A

Proliferation of neoplastic plasma cells

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152
Q

Most common primary malignant tumour of bone in adults

A

Multiple myeloma

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153
Q

Treatment of multiple myeloma

A

Chemotherapy, bisphosphonates, radiation,s surgery for symptomatic lesions or impending fractures - debulking, internal fixation

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154
Q

Diagnosis of multiple myeloma

A
  • serum/urine immunoelectrophoresis (monoclonal gammopathy)

- CT-guided biopsy of lytic lesions at multiple bony sites

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155
Q

Radiographic findings of multiple myeloma

A

Multiple, “punched-out” well-demarcated lesions, no surrounding sclerosis, marked bone expansion

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156
Q

Signs and symptoms of multiple myeloma

A

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)

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157
Q

Labs for multiple myeloma

A

Anemia, thrombocytopenia, increased ESR, hypercalcemia, increased Cr

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158
Q

Risk factors for neck pain?

A
  • Non-modifiable: F, middle-age, occupation, more children
  • Modifiable: smoking/enviro tobacco, inactivity, occupational.
  • Others: psychology (depression, anxiety, poor coping skills), trauma (TBI)
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159
Q

Etiology of neck pain

A
  • Mechanical – strain, whiplash, DDD, OA
  • Traumatic – fracture, ligamentous
  • Neurological – stenosis, radiculopathy, myelopathy
  • Inflammatory – RA, PMR
  • Infectious, malignant, metabolic
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160
Q

Investigations for neck pain

A
  • X-ray – In the absence of red flags - imaging is not necessary in patients with mild acute or chronic neck pain that does not limit or interrupt daily activities, does not affect performance of occupation, and is easily ignored when distracted
  • MRI - should be performed urgently in patients suspected of having an infection, malignancy, or spinal cord compression
  • Infection: White blood cell (WBC) count, CRP, imaging (usually MRI or CT), and culture of infected tissue
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161
Q

Treatment for neck pain

A
  • Spinal Manipulation – short term evidence that it is helpful
  • Acupuncture – good for muscle based pain
  • Massage – superior to no treatment
  • Exercise Therapy – strong evidence
  • Surgery – Used for radiculopathy, NOT neck pain
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162
Q

Questions to ask on history for neck pain

A
  • OPQRST - changes in position, weight bearing, and time of day (eg, at night, when awakening), previous problems
  • Stiffness, numbness, paresthesias, weakness, concussion (WAD)
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163
Q

Physical exam for neck pain

A
  • Spinal examination: visible deformity, area of erythema, or vesicular rash,
  • Neuro: muscle strength, sensory, reflex and gait testing, and evaluation for upper motor neuron signs
  • Neck: range of motion (rotation and lateral flexion), palpation of the trapezius and paraspinal muscles
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164
Q

Symptoms of C4 radiculopathy

A

Pain in the lower neck and trapezius area with paresthesias involving the lower neck and upper shoulder girdle

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165
Q

Symptoms of C5 radiculopathy

A
  • Pain in neck, shoulder, and dorsal forearm with paresthesias and numbness involving the dorsal arm
  • Weakness of deltoid, biceps, rotator cuff
  • Decrease in the biceps reflex
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166
Q

Symptoms of C6 radiculopathy

A
  • Pain in the trapezius ridge and tip of the shoulder, often radiating to the thumb and index finger, with paresthesias and numbness in the same areas
  • Weakness of the wrist extensors
  • Decreased brachioradialis reflexes
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167
Q

Symptoms of C7 radiculopathy

A
  • Pain, paresthesias, and numbness in the shoulder blade and axilla, radiating to the long and ring fingers
  • Weakness of triceps
  • Decreased triceps brachii reflex
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168
Q

Red flags for neck pain?

A
  • Neck pain associated with lower extremity weakness, gait or coordination difficulties, and/or bladder or bowel dysfunction
  • A shock-like paresthesia occurring with neck flexion (Lhermitte’s sign)
  • Fever
  • Unexplained weight loss
  • Headache, vision changes
  • Anterior neck pain
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169
Q

Definition of whiplash associated disorders?

A

Whiplash injury is defined as neck injury resulting from an acceleration-deceleration mechanism that causes sudden extension and flexion of the neck

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170
Q

Symptoms of whiplash associated disorders?

A
  • Neck pain and stiffness which may present immediately after the injury or may be delayed for several days
  • Associated WAD symptoms: tinnitus, headache, dizziness, memory loss, TMJ pain.
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171
Q

Classification of whiplash associated disorders?

A
  • Grade 0: no complaints about neck, no physical signs. Treat: reassure.
  • Grade 1: pain/stiffness or tenderness only, full ROM (no physical signs). Treat: pain relief.
  • Grade 2: pain/stiffness or tenderness, MSK SIGNS on physical exam (ROM, tenderness). Treat: prompt investigation.
  • Grade 3: neck complaints with NEURO SIGNS on physical exam – reflexes, weakness, numbness. Treat: prompt investigation.
  • Grade 4: neck complaint with fracture/dislocation. Treat: prompt investigation.
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172
Q

What should you include in the description of fractures?

A
  • Site
  • Open vs. closed
  • Length
  • Articular
  • Rotation
  • Translation
  • Alignment/Angulation
  • Type e.g. Salter-Harris, etc.
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173
Q

Indications for open reduction for fractures?

A

“NO CAST”

  • Non-union
  • Open fracture
  • Neurovascular Compromise
  • Displaced intra-Articular fracture
  • Salter-Harris 3,4,5
  • PolyTrauma
174
Q

Definition of open fractures?

A

Communication between fracture site and external surface of skin – increased risk of osteomyelitis

175
Q

Management of open fractures?

A
  • Remove gross debris, irrigate, cover with sterile dressing - formal irrigation and debridement often done in the OR
  • Control bleeding with pressure (no clamping)
  • Splint
  • Antibiotics (1st generation cephalosporin and aminoglycoside) and tetanus prophylaxis
  • Standard of care is to secure definitive surgical management within 6h
176
Q

MOA of anterior shoulder dislocation?

A

Abducted arm is externally rotated/hyperextended; Blow to posterior shoulder

177
Q

Symptoms of anterior shoulder dislocation?

A

Pain, arm slightly abducted and externally rotated with inability to internally rotate

178
Q

Shoulder exam findings for anterior shoulder dislocation?

A
  • “Squared off” shoulder
  • Positive apprehension test
  • Positive relocation test
  • Positive sulcus sign
179
Q

What is a Hill-Sachs lesion

A

Compression fracture of posterior humeral head due to forceful impaction of an anteriorly dislocated humeral head against the glenoid rim

180
Q

What is a bony bankart lesion?

A

Avulsion of the anterior glenoid labrum (with attached bone fragments) from the glenoid rim

181
Q

Treatment of anterior shoulder dislocation?

A
  • Closed reduction with IV sedation and muscle relaxation
  • Traction-countertraction: assistant stabilizes torso with a folded sheet wrapped across the chest while the surgeon applies gentle steady traction
182
Q

What should be done on neurovascular exam for anterior shoulder dislocation?

A
  • Axillary nerve: sensory patch over deltoid and deltoid contraction
  • Musculocutaneous nerve: sensory patch on lateral forearm and biceps contraction
183
Q

MOA of posterior shoulder dislocation?

A
  • Adducted, internally rotated, flexed arm FOOSH

- 3 Es (epileptic seizure, EtOH, electrocution)

184
Q

Symptoms of posterior shoulder dislocation?

A

Pain, arm is held in adduction and internal rotation; external rotation is blocked

185
Q

Shoulder exam findings for posterior shoulder dislocation?

A
  • Anterior shoulder flattening, prominent coracoid, palpable mass posterior to shoulder
  • Positive posterior apprehension (“jerk”) test
186
Q

Treatment of posterior shoulder dislocation?

A
  • Closed reduction with sedation and muscle relaxation Inferior traction on a flexed elbow with pressure on the back of the humeral head
  • Obtain post-reduction x-rays
  • Check post-reduction NVS
  • Sling in abduction and external rotation x 3 wk, followed by shoulder rehabilitation (dynamic stabilizer strengthening)
187
Q

What is the posterior apprehension (“jerk”) test?

A

With patient supine, flex elbow 90° and adduct, internally rotate the arm while applying a posterior force to the shoulder; patient will “jerk” back with the sensation of subluxation

188
Q

MOA for acromioclavicular joint pathology

A

Fall onto shoulder with adducted arm or direct trauma to point of shoulder

189
Q

Clinical features of acromioclavicular joint pathology

A
  • Pain with adduction of shoulder and/or palpation over AC joint
  • Palpable step deformity between distal clavicle and acromion (with dislocation) i.e. piano key sign
  • Limited ROM
190
Q

Indication for operative treatment for acromioclavicular joint pathology

A

Rockwood Class IV-VI (III if labourer or high level athlete)

191
Q

Non-operative treatment for acromioclavicular joint pathology

A

Sling 1-3 wk, ice, analgesia, early ROM and rehabilitation

192
Q

MOA for clavicle fracture?

A

Fall on shoulder (87%), direct trauma to clavicle (7%), FOOSH (6%)

193
Q

Clinical features of clavicle fracture?

A
  • Pain and tenting of skin

- Arm is clasped to chest to splint shoulder and prevent movement

194
Q

Treatment for medial and middle-third clavicle fractures

A
  • for nondisplaced fractures, simple sling x 1-2 wk prn
  • early ROM and strengthening once pain subsides
  • if fracture is shortened >2 cm, consider ORIF
195
Q

Treatment for distal-third clavicle fractures

A
  • undisplaced (with ligaments intact): sling x 1-2 wk

- displaced (CC ligament injury): ORIF

196
Q

MOA of proximal humeral fractures?

A
  • young: high energy trauma (MVC)

- elderly: FOOSH from standing height in osteoporotic individuals

197
Q

Clinical features of proximal humeral fractures?

A

Proximal humeral tenderness, deformity with severe fracture, swelling, painful ROM - – do PASSIVE ROM initially to avoid rotator cuff pulling on ligaments, bruising extends down arm and chest

198
Q

Investigations for proximal humeral fractures?

A
  • Test axillary nerve function (deltoid contraction and skin over deltoid)
  • X-rays: AP, trans-scapular, and axillary views of the shoulder are essential
  • CT scan: to evaluate for articular involvement and fracture displacement
199
Q

Classification system used for proximal humeral fractures?

A

Neer classification is based on 4 fracture locations or ‘parts’

200
Q

MOA of humeral shaft fractures?

A

High energy: direct blows/MVC (especially young); low energy: FOOSH, twisting injuries, metastases (in elderly)

201
Q

Non-operative treatment of proximal humeral fractures?

A
  • nondisplaced and minimally displaced (85% of patients): broad arm sling immobilization, begin ROM within 14 d to prevent stiffness
  • most displaced fractures in low-demand elderly patients
202
Q

Operative treatment of proximal humeral fractures?

A
  • ORIF (anatomic neck fractures, displaced, associated irreducible glenohumeral joint dislocation)
  • hemiarthroplasty or reverse TSA may be necessary, especially in elderly
203
Q

Clinical features of humeral shaft fractures?

A
  • Pain, swelling, weakness ± shortening, motion/crepitus at fracture site
  • Must test radial nerve function before and after treatment: look for drop wrist, sensory impairment in dorsum of hand
204
Q

Investigations for humeral shaft fractures?

A

X-ray: AP and lateral views of the humerus, including the shoulder and elbow joints

205
Q

Indications for operative treatment for humeral shaft fractures?

A

“NOCAST” ,pathological fracture, “floating elbow” (simultaneous unstable humeral and forearm fractures)

206
Q

Non-operative treatment for humeral shaft fractures?

A
  • ± reduction; can accept deformity due to compensatory ROM of shoulder
  • hanging cast (weight of arm in cast provides traction across fracture site) with collar and cuff sling immobilization until swelling subsides, then Sarmiento functional brace, followed by ROM
207
Q

Operative treatment for humeral shaft fractures?

A

ORIF: plating (most common), IM rod insertion, external fixation

208
Q

MOA for distal humeral fracture?

A
  • young: high energy trauma (MVC)

- elderly: FOOSH

209
Q

Clinical features of distal humeral fracture?

A
  • Elbow pain and swelling

- Assess brachial artery

210
Q

Investigations for distal humeral fracture?

A
  • X-ray: AP and lateral views of the humerus and elbow
  • CT scan: helpful when suspecting shear fracture of capitulum or trochlea
  • Assess NVS: radial, ulnar and median nerve
211
Q

What population receives non-operative treatment for distal humeral fracture?

A

Pediatric patients only

212
Q

Operative indications for distal humeral fracture?

A

Displaced, supracondylar, bicolumnar

213
Q

Non-operative treatment for distal humeral fracture?

A

Cast immobilization (in supination for lateral condyle fracture; pronation for medial condyle fractures)

214
Q

Operative treatment for distal humeral fracture?

A
  • closed reduction and percutaneous pinning (children); ORIF; total elbow arthroplasty (bicolumnar in elderly)
  • adult fractures are almost always treated operatively due to risk of elbow stiffness with non-operative
215
Q

For distal humeral fracture, goal is to restore ROM to ___

A

30-130° flexion

216
Q

Subclass of distal humerus fracture: extra-articular, fracture proximal to capitulum and trochlea, usually transverse

A

Supracondylar fracture

217
Q

Clinical features of supracondylar fracture?

A
  • pain, swelling, point tenderness

- neurovascular injury: median and radial nerves, radial artery

218
Q

Xray findings for supracondylar fracture?

A
  • Disruption of anterior humeral line suggests supracondylar fracture
  • Fat pad sign: a sign of effusion and can be indicative of occult fracture
219
Q

Non-operative treatment for supracondylar fracture?

A

Nondisplaced (pediatric): long arm plaster slab in 90 flexion x 3 wk

220
Q

Operative indications for supracondylar fracture?

A

Displaced >50%, vascular injury, open fracture

221
Q

Operative treatment for supracondylar fracture?

A
  • requires percutaneous pinning followed by limb cast with elbow flexed <90
  • in adults, ORIF is necessary
222
Q

Investigations for supracondylar fracture?

A
  • X-ray: AP and lateral views of the elbow

- Assess NVS: median and radial nerves, radial artery

223
Q

MOA of anterior hip dislocations?

A

Posteriorly directed blow to knee with hip widely abducted

224
Q

Clinical features of anterior hip dislocations?

A

Shortened, abducted, externally rotated limb

225
Q

Treatment of anterior hip dislocations?

A
  • closed reduction under conscious sedation/GA

- post-reduction CT to assess joint congruity

226
Q

Most frequent type of hip dislocation

A

Posterior hip dislocation

227
Q

MOA of posterior hip dislocation

A

Severe force to knee with hip flexed and adducted e.g. knee into dashboard in MVC

228
Q

Clinical features of posterior hip dislocation

A

Shortened, adducted, internally rotated limb

229
Q

Treatment of posterior hip dislocation

A
  • closed reduction under conscious sedation/GA only if no associated femoral neck fracture or ipsilateral displacement
  • ORIF if unstable, intra-articular fragments, or posterior wall fracture
  • post-reduction CT to assess joint congruity and fractures
  • if reduction is unstable, put in traction x 4-6 wk
230
Q

Types of hip fractures?

A
  • Femoral Neck (Subcapital)
  • Intertrochanteric
  • Subtrochanteric
231
Q

Treatment of femoral neck fractures

A
  • Garden I, II: internal fixation to prevent displacement
  • Garden III, IV: young: ORIF, old: hemi-/total hip arthroplasty
  • The goal is rigid early fixation to allow early weight bearing and mobilization – want them standing and walking within first 24 hours after injury
232
Q

Treatment of intertrochanteric femoral fractures

A

Closed reduction under fluoroscopy then dynamic hip screw or IM nail

233
Q

Treatment of subtrochanteric femoral fractures

A

Closed/open under fluoroscopy, then plate fixation or IM nail

234
Q

Complications of hip fractures?

A

DVT, non-union, AVN, dislocation

235
Q

MOA for ACL tear?

A

Usually non-contact, decel, landing from jump or pivot/changing direction

236
Q

History of ACL tear?

A
  • Audible “pop”
  • Immediate swelling
  • Knee “giving way”
  • Inability to continue activity
237
Q

Physical exam findings of ACL tear?

A
  • Effusion (hemarthrosis)
  • Posterolateral joint line tenderness
  • Positive anterior drawer
  • Positive Lachmann
  • Pivot shift
  • Test for MCL, meniscal injuries
238
Q

What injury is commonly associated with ACL tears acutely and chronically?

A

Concurrent lateral meniscal tear is common acutely, but medial chronically

239
Q

What is a second fracture?

A

Avulsion fracture (small) of the lateral surface of the lateral tibial condyle. Usually results from excessive internal rotation and varus stress resulting in increased tension on the lateral capsular ligament of the knee joint. Pathognomonic for ACL tear.

240
Q

Treatment of ACL tear

A
  • Stable knee with minimal functional impairment: immobilization 2-4 wk with early ROM and strengthening
  • High demand lifestyle: ligament reconstruction
241
Q

MOA of PCL tear?

A

Sudden posterior displacement of tibia when knee is flexed or hyperextended (e.g. dashboard MVC injury)

242
Q

History for PCL tear?

A
  • Audible “pop”
  • Immediate swelling
  • Pain with push off
  • Cannot descend stairs
243
Q

Physical exam findings for PCL tear?

A
  • Effusion (hemarthrosis)
  • Anteromedial joint line tenderness
  • Positive posterior drawer
  • Reverse pivot shift
  • Other ligamentous, bony injuries
244
Q

Treatment of PCL tear?

A
  • Unstable knee or young person/high-demand lifestyle: ligament reconstruction
  • Most people can cope with being PCL deficient.
245
Q

MOA for MCL tear?

A

Valgus force to knee = MCL tear

246
Q

MOA for LCL tear?

A

Varus force to knee = LCL tear

247
Q

O’Donoghue’s unhappy triad

A
  • ACL rupture
  • MCL rupture
  • Meniscal damage (medial and/or lateral)
248
Q

Clinical features of MCL + LCL tears?

A
  • Swelling/effusion - If there is large effusion present, think about ACL tear because MCL tears don’t usually cause effusions.
  • Tenderness above and below joint line medially (MCL) or laterally (LCL)
  • Joint laxity with varus or valgus force to knee
  • laxity with endpoint suggests partial tear
  • laxity with no endpoint suggests a complete tear
  • Test for other injuries (e.g. O’Donoghue’s unhappy triad), common peroneal nerve injury
249
Q

Treatment of MCL + LCL tears?

A
  • Partial tear: immobilization x 2-4 wk with early ROM and strengthening
  • Complete tear: immobilization at 30° flexion
250
Q

MOA of meniscal tear

A

Twisting force on knee when it is partially flexed (e.g. stepping down and turning)

251
Q

Lateral meniscal tear is associated with ___ injury but medial ones are associated with ___ tear.

A

Acute ACL

Chronic ACL

252
Q

Clinical features of meniscal tear

A
  • Immediate pain, difficulty weight-bearing, instability, and clicking
  • Increased pain with squatting and/or twisting
  • Effusion (hemarthrosis) with insidious onset (24-48h after injury)
  • Joint line tenderness medially or laterally
  • Locking of knee (if portion of meniscus mechanically obstructing extension)
253
Q

Non-operative indication for meniscal tear?

A

Not locked

254
Q

Non-operative treatment for meniscal tear?

A

ROM and strengthening (NSAIDs)

255
Q

Operative indication for meniscal tear?

A
  • Locked (i.e. patient cannot fully extend knee, due to mechanical block) or failed non-operative treatment
  • Meniscal repair is done if tear is peripheral with good vascular supply, is a longitudinal tear and 1-4 cm in length
256
Q

Operative treatment for meniscal tear?

A

Arthroscopic repair/partial meniscectomy - Partial meniscectomy is done with tears not amenable to repair (complex, degenerative, radial)

257
Q

MOA for quad/patellar tendon rupture?

A
  • Sudden forceful contraction of quadriceps during an attempt to stop
  • More common in obese patients and those with pre-existing degenerative changes in tendon
258
Q

Risk factors for quad/patellar tendon rupture?

A

DM, SLE, RA, steroid use, renal failure on dialysis

259
Q

Clinical features for quad/patellar tendon rupture?

A
  • Inability to extend knee or weight-bear
  • Possible audible “pop”
  • Patella in lower or higher position with palpable gap above or below patella, respectively
  • May have an effusion
260
Q

Investigations for quad/patellar tendon rupture?

A
  • Perform straight leg raise (unable to with complete rupture)
  • Knee X-ray to rule out patellar fracture, MRI to distinguish between complete and partial tears
  • Lateral view: patella alta with patella tendon rupture, patella baja (infera) with quadriceps tendon rupture
261
Q

Non-operative indications for quad/patellar tendon rupture?

A

Incomplete tears with preserved extension of knee

262
Q

Non-operative treatment for quad/patellar tendon rupture?

A

Immobilization in brace

263
Q

Operative indications for quad/patellar tendon rupture?

A

Complete ruptures with loss of extensor mechanism

264
Q

Clinical features of knee dislocation?

A
  • Classified by relation of tibia with respect to femur: anterior, posterior, lateral, medial, rotary
  • knee instability
  • effusion
  • pain
  • ischemic limb
265
Q

Investigations for knee dislocation?

A
  1. X-ray: AP, lateral, and skyline views of the knee
    - associated radiographic findings include tibial plateau fracture dislocations, proximal fibular fractures, and avulsion of fibular head
  2. Assessment of NVS:
    - ABI (abnormal if <0.9)
    - arteriogram or CT angiogram if abnormal vascular exam (such as abnormal pedal pulses)
    - assessment of peroneal nerve, tibial artery, and ligamentous injuries
266
Q

Treatment for knee dislocation?

A
  • Urgent closed reduction
  • Assessment of peroneal nerve, tibial artery, and ligamentous injuries
  • Emergent operative repair if vascular injury, open fracture or dislocation, irreducible dislocation, compartment syndrome
  • Knee immobilization x6-8wk
267
Q

MOA for patellar fracture

A

Direct blow to the patella: fall, MVC (dashboard)

268
Q

Clinical features for patellar fracture

A
  • Marked tenderness
  • Inability to extend knee or straight leg raise
  • Proximal displacement of patella
  • Patellar deformity
  • ± effusion/hemarthrosis
269
Q

Investigations for patellar fracture

A
  • X-rays: AP, lateral, skyline
  • Do not confuse with bipartite patella: congenitally unfused ossification centres with smooth margins on X-ray at superolateral corner
270
Q

Non-operative indications for patellar fracture

A

Non-displaced (step-off <2-3 mm and fracture gap <1-4 mm)

271
Q

Operative indications for patellar fracture

A

Displaced (>2 mm), comminuted, disrupted extensor mechanism

272
Q

Non-operative treatment for patellar fracture

A
  • Straight leg immobilization 1-4wk with hinged knee brace, weight bearing as tolerated
  • Progress in flexion after 2-3wk
  • physiotherapy: quadriceps strengthening when pain has subsided
273
Q

Operative treatment for patellar fracture

A

ORIF, if comminuted may require partial/complete patellectomy

274
Q

MOA for patellar dislocation

A
  • Usually a non-contact twisting injury
  • Lateral displacement of patella after contraction of quadriceps at the start of knee flexion in an almost straight knee joint
275
Q

Risk factors for patellar dislocation

A
  • young, female
  • obesity
  • high-riding patella (patella alta)
  • genu valgus
  • Q-angle (quadriceps angle) >20
  • Shallow intercondylar groove
  • weak vastus medialis
  • tight lateral retinaculum
  • ligamentous laxity (Ehlers-Danlos)
276
Q

MOA of tibial shaft fracture

A
  • Low energy pattern: torsional injury

- High energy: including MVC, falls, sporting injuries

277
Q

Clinical features of patellar dislocation

A
  • Knee catches or gives way with walking
  • Severe pain, tenderness anteromedially from rupture of capsule
  • Weak knee extension or inability to extend leg unless patella reduced
  • Positive patellar apprehension test
  • increased Q-angle
  • J-sign
278
Q

What is the J sign

A

Associated with patella alta; increased lateral translation in extension which pops into the patellofemoal groove as the patella engages the trochlea early in flexion

279
Q

Non-operative treatment for patellar dislocation?

A
  • NSAIDs, activity modification, and physical therapy
  • short-term immobilization for comfort, then 6 wk controlled motion
  • progressive weight bearing and isometric quadriceps strengthening – try to strengthen VMO (vastus medius obliquus)
280
Q

Operative treatment for patellar dislocation?

A

Surgical tightening of medial capsule and release of lateral retinaculum, possible tibial tuberosity transfer, or proximal tibial osteotomy

281
Q

Operative indications for patellar dislocation?

A

If recurrent or if loose bodies present

282
Q

Clinical features of tibial shaft fracture

A
  • Pain, inability to weight bear
  • Open vs. closed
  • Neurovascular compromise
283
Q

Investigations of tibial shaft fracture

A
  • X-ray: AP and lateral views: full length, plus knee and ankle
284
Q

Non-operative indications for tibial shaft fracture

A

Closed and minimally displaced or adequate closed reduction

285
Q

Operative indications for tibial shaft fracture

A

Displaced or open

286
Q

Non-operative treatment for tibial shaft fracture

A

Long leg cast x8-12wk, functional brace after

287
Q

Operative treatment for tibial shaft fracture

A
  • if displaced and closed: ORIF with IM nail, plate and screws, or external fixator
  • if open: antibiotics, I&D, external fixation or IM nail, and vascularized coverage of soft tissue defects
288
Q

Operative indications for ankle fracture

A
  • any fracture-dislocation: restore vascularity, minimize articular injury, reduce pain and skin pressure
  • most of type B, and all of type C
  • trimalleolar (medial, posterior, lateral) fractures
  • talar tilt >10
  • medial clear space on X-ray greater than superior clear space
  • open fracture/open joint injury
289
Q

Operative treatment for ankle fracture

A

ORIF

290
Q

Non-operative indications for ankle fracture

A

Non-displaced, no history of dislocation

291
Q

Non-operative treatment for ankle fracture

A

Below knee cast, NWB, or aircast WBAT

292
Q

Treatment for microscopic tear (Grade I) ankle ligamentous injuries?

A
  • rest, ice, compression, elevation
293
Q

Treatment for macroscopic tear (Grade II) ankle ligamentous injuries?

A
  • strap ankle in dorsiflexion and eversion x 4-6 wk

- physiotherapy: strengthening and proprioceptive retraining

294
Q

Treatment for complete tear (Grade III) ankle ligamentous injuries?

A
  • below knee walking cast x 4-6 wk
  • physiotherapy: strengthening and proprioceptive retraining
  • surgical intervention may be required if chronic symptomatic instability develops
295
Q

Inversion ankle ligamentous injury, >90% of all ankle sprains

A

Lateral ligament complex

296
Q

Eversion ankle ligamentous injury?

A

Medial ligament complex (deltoid ligament)

297
Q

Clinical features of lateral ligament ankle complex injury

A
  • Swelling and tenderness anterior to lateral malleolus
  • ++ ecchymosis
  • Positive ankle anterior drawer
298
Q

In Weber’s classification of ankle fractures what is Type A?

A

Below level of talar dome very distal fibula, usually transverse

299
Q

In Weber’s classification of ankle fractures what is Type B?

A

At level of joint, widening of distal tibiofibular joint indicating syndesmotic injury, medial malleolus may be fractured

300
Q

In Weber’s classification of ankle fractures what is Type C?

A

Above the level of ankle joint, tibiofibular syndesmosis is disrupted, medial malleolus fracture or deltoid ligament injury, worst stability

301
Q

MOA for talar fractures

A

Axial loading or hyperdorsiflexion (MVC, fall from height)

302
Q

Investigations for talar fractures

A

AP, lateral, Canale view (XRay), CT (better characterize the fracture), MRI (define AVN extent)

303
Q

Non-operative indications for talar fractures

A

Non-displaced

304
Q

Non-operative treatment for talar fractures

A

NWB, below-knee cast x 6wks

305
Q

Operative indications for talar fractures

A

Displaced

306
Q

High risk for __ with displaced talar fractures

A

AVN

307
Q

Operative treatment for talar fractures

A

ORIF - high rate of nonunion, AVN – neck fracture: ORIF

308
Q

Most common tarsal fracture

A

Calcaneal fracture

309
Q

MOA for calcaneal fracture

A

High energy axial loading (fall from height onto heels)

310
Q

Symptoms and signs for calcaneal fracture

A

Marked swelling, bruising on heel/sole – wider, shortened, flatter heel if viewed from behind, varus heel

311
Q

What is a Haglund deformity?

A

Enlargement of the posterior-superior tuberosity of the calcaneus

312
Q

Investigations for calcaneal fracture

A

AP, lateral, oblique foot (mandatory view); can also assess with Broden view, Harris view, or AP ankle – loss of Bohler’s angle, CT (gold standard to assess intra-articular extension)

313
Q

Treatment of calcaneal fracture

A

Reduction, NWB cast x 3 months with early ROM and strengthening; avoid wound complications, restore articular congruity and normal calcaneal width and height – maximum functional recovery may take longer than 12 months

314
Q

Definition of psoriatic arthritis?

A

Arthritic inflammation associated with psoriasis

315
Q

Signs and symptoms of psoriatic arthritis?

A
  1. Dermatologic
    - well-demarcated erythematous plaques with silvery scale
    - nail involvement: pitting, transverse or longitudinal ridging, discolouration, subungual hyperkeratosis, onycholysis, and oil drops o musculoskeletal
    - other findings: dactylitis, enthesopathy, morning stiffness >30 min (50%)
  2. Ophthalmic
    - conjunctivitis, iritis (anterior uveitis)
  3. Cardiac and respiratory (late findings)
    - aortic insufficiency
    - apical lung fibrosis
  4. Neurologic
    - cauda equina syndrome
  5. Radiologic
    - floating syndesmophytes
    - pencil-in-cup appearance at IP joints
    - osteolysis, periostitis
316
Q

5 subtypes of psoriatic arthritis?

A
  • Sacroiliitis, Spondylitis (usually older, male patients)
  • Asymmetric oligoarthritis (70%)
  • DIP arthritis
  • Symmetrical polyarthritis (similar to RA)
  • Arthritis mutilans (destructive and deforming small joint polyarthritis)
317
Q

Treatment of psoriatic arthritis?

A
  • Treat skin lesions (e.g. steroid cream, salicylic and/or retinoic acid, tar, UV light)
  • NSAIDs or IA steroids (benefit should be seen within a few weeks, should not be the sole therapy >3mo)
  • DMARDs to minimize erosive disease (use early in peripheral joint involvement)
  • Biologic therapies include anti-TNF agents, anti-IL-17 (secukinumab), and anti-IL-12/23 (ustekinumab)
318
Q

What are the symptoms of systemic lupus erythematosus (SLE)?

A

SOAP BRAIN MD: include fever, rash (malar rash - erythematous, raised lesions with sparing of nasal folds, discoid rash subcutaneous forms→ annular plaques), photosensitivity (rash lasts weeks), alopecia (discoid lupus → hyperkeratosis plugs up hair follicle), oral/nasal ulceration, arthritis (small joint, inflammatory, polyarthritis – need 2 or more joints, not erosive), serositis, renal disease, hematological disease (cytopenia, anemia, lymphopenia, leukopenia, ITP), neurological disease (seizures, psychosis)

319
Q

How many SOAP BRAIN MD symptoms do you need for SLE diagnosis?

A

4

320
Q

Investigations for SLE?

A

Anti-nuclear Abs (ANA) positive in 99% SLE patients (but 5% normal), anti-ds DNA and anti-Smith (Sm) antibodies more specific to SLE

321
Q

Is SLE more common in females or males?

A

More likely in females (estrogen)

322
Q

Treatment of SLE?

A

Respond to DMARDs similar to RA; anti-malarial medications*, topical + systemic corticosteroids, immunosuppressive/cytotoxic agents if severe (cyclophosphamide), supportive care (antihypertensives, Ca channel blockers for Raynaud’s, photoprotection)

323
Q

Risk factors for RA?

A

Age >50, female (3:1), first degree relative with rheumatoid arthritis, smoking, low level of education

324
Q

Pathophysiology of RA

A

Destruction mediated process - proteases produced by synovial cells destroy proteoglycans in the articular cartilage - irreversible damage 6 months to 1 year from disease onset

325
Q

Definition of RA

A

Rheumatoid arthritis is a systemic inflammatory disease characterized by symmetric, relapsing, or chronic destructive synovitis. There may also be multisystem involvement.

326
Q

Triggers of RA?

A

Viruses (Parvovirus, EBV, HTLV), super antigens (from bacteria/viruses), auto antigens (QKRAA)

327
Q

Epidemiology of RA?

A

The condition is more common in women, with onset between ages 30 and 60 years.

328
Q

Classic sites for RA?

A
  1. HANDS
    - MCP, PIP, and wrist joints most commonly involved
    - DIP SPARING
  2. FEET
    - MTP joint involved
  3. LEGS knees (80%), ankles (80%), hips (50%)
  4. ARMS shoulders (60%), elbows (50%), acromioclavicular (50%)
  5. ATLANTOAXIAL (C1, C2) subluxation may lead to spinal cord (cervical myelopathy with hand weakness/numbness)
  6. TEMPOROMANDIBULAR (30%)
329
Q

Symptoms of RA?

A
  • History of pain and stiffness in multiple joints with initial symptoms predominantly at 1 location or a few scattered sites and fatigue, weight loss, and myalgia.
  • The most common presentation is the insidious development of arthralgia, arthritis, malaise, and fatigue over several weeks, however, an acute polyarticular development over a few days is possible.
  • Morning stiffness (gelling) usually lasting > 30 minutes is a common feature and is usually relieved with activity and warmth.
330
Q

Physical exam findings of hands and feet of RA

A
  1. Hands: Deformities include Boutonniere, swan neck, Z (thumb), ulnar deviation at MCP joint, volar subluxation of proximal phalanx from MCP head, radial deviation of carpus, compression of the carpal bones, subluxation at the wrist
  2. Feet: Deformities include valgus of the ankle and hindfoot, pes planus, forefoot varus and hallux valgus, cock up toes
331
Q

Xray findings of RA?

A

X rays of affected joints (particularly hands, knees, and ankles; soft tissue swelling, periarticular osteopenia, narrowing of joint space, marginal bony erosions, subluxation, joint destruction, bony ankylosis) – good to have a baseline for follow-up

332
Q

Investigations for RA?

A
  • LABS: CBCD, lytes, urea, Cr, AST, ALT, ALP, bilirubin, ESR, CRP, RF (IgM), anti CCP (most specific), ANA, urinalysis
  • Patients frequently anemic, inflammatory markers may be normal, high platelets
  • INFECTIOUS WORKUP serologies (Parvovirus, HBV, HCV, EBV, CMV, Borrelia burgdorferi)
333
Q

Prior to starting DMARDs for RA what should you screen for?

A

Screen for hepatitis B, hepatitis C, and latent tuberculosis infections, give all age-/risk-appropriate immunizations

334
Q

___ are recommended as first-line therapy for RA and should be started early in the diseases course.

A

DMARDs
- In most patients, begin DMARD therapy with either methotrexate 10-25 mg once weekly or leflunomide 10-20 mg/day orally.

335
Q

Adjunct pharmacological therapy for RA

A
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) orally or topically may help to control symptoms but are not disease modifying.
  • Corticosteroids orally or intra-articularly may be used for symptom control. Early low-dose steroids added to DMARD therapy may be used to reduce joint destruction and increase clinical remission rates.
336
Q

Nonpharmacologic patient management of RA

A

Patient education, exercise, physical and occupational therapies, and cognitive therapies.

337
Q

Predisposing factors to septic joint?

A

Advance age, Pre-existing joint disease, Recent joint surgery or injection, Skin or soft tissue infection, Intravenous drug use, Indwelling catheters, Immunosuppression (including diabetes)

338
Q

Most common mechanism of infect for septic joint?

A

Most commonly, septic arthritis arises via hematogenous seeding of the synovial membrane (which has no limiting basement membrane, thus allowing organisms to enter the joint space). Septic arthritis due to hematogenous seeding is most commonly caused by organisms with propensity to adhere to the synovial tissues (such as Staphylococcus aureus)

339
Q

Most common bacteria of septic joint?

A

S. aureus (including methicillin-resistant S. aureus) is the most common cause of septic arthritis in adults.

340
Q

Signs and symptoms of septic joint?

A
  • Joint pain, swelling, warmth, and restricted movement occur in 80 percent of patients with septic arthritis. Most patients are febrile
  • The knee is involved in more than 50 percent of cases; wrists, ankles, and hips are also affected commonly
341
Q

The diagnosis of septic arthritis should be suspected in patients with

A

Acute onset of at least one swollen, painful joint, with or without relevant risk factors (including bacteremia, pre-existing joint disease, and immunosuppression).

342
Q

The diagnosis of septic arthritis is made based on synovial fluid analysis and culture:

A
  • Cell count = >50,000
  • Polys = >75%
  • Crystals = none
  • Gm stain and culture = positive
343
Q

what should the synovial fluid be sent for if suspecting septic joint?

A

Synovial fluid should be sent for Gram stain, bacterial culture, white blood cell count with differential, and assessment for crystals (monosodium urate and calcium pyrophosphate crystal deposition crystals) with a polarizing microscope.

344
Q

Treatment of septic joint

A
  • Joint drainage — In general, patients with septic arthritis warrant joint drainage, since this condition represents a closed abscess. Approaches to joint drainage for management of septic arthritis in adults include needle aspiration, arthroscopic drainage, or arthrotomy (open surgical drainage). Treat till at least 2 negative cultures
  • Antibiotics - If the initial Gram stain of synovial fluid demonstrates gram-positive cocci, empiric treatment with vancomycin (15 to 20 mg/kg/dose intravenously [IV] every 8 to 12 hours) should be administered for 2 weeks
345
Q

Most common sites of gout?

A

1st MTP – podagra, feet, ankles, knees also common

346
Q

Risk factors for gout?

A

Male, obese, >40yo, HTN, EtOH, family Hx, renal failure, leukemia (tumor lysis syndrome), metabolic abnormalities

347
Q

Triggers for gout?

A
  • Fluid shifts (diuretics, low dose ASA, illness, surgery)
  • High cell turnover/chemo
  • Diets high in meat/seafood
  • EtOH
  • Starting or stopping allopurinol (do not give/take away in acute phase)
348
Q

Stages of gout?

A
  1. Asymptomatic hyperuricemia (elevated uric acid, no gouty attacks)
  2. Acute gouty arthritis
  3. Intercritical gout (asymp between flares)
  4. Chronic tophaceous gout
349
Q

Presentation of gout

A

Recurrent acute mono/oligoarthritis. Extreme pain, red, hot and swollen, typically subsides in 3-10 d.

350
Q

During a gout flare should the blood be hyperuricemic

A

In blood, there is serum hyperuricemia that elevations postmenopause in women and after puberty with men however NOT DURING A FLARE (since all of it goes into the joints). During a flare the blood test should be normal and when not, it should be hyperuricemic!

351
Q

Pathophysiology of gout?

A

IMBALANCE decreased urate excretion and/or increased urate production - uric acid crystals deposited in joints, skin, and kidneys - arthritis, tophi, and renal failure.

352
Q

Diagnosis of gout?

A
  • Arthrocentesis (aspiration): Urate crystals microscopy/polarized light - negatively birefringent, needle shaped. MUST rule out septic arthritis (infected joints can have crystals present)
  • Radiology: soft tissue swelling, if chronic→ tophi + bone erosions “punched out”, rocker bottom shoes
353
Q

Treatment of gout?

A
  • Intra-articular steroid injection - Methylprednisolone 100 150 mg intra articularly once
  • Colchicine - microtubule interference to prevent inflammation. 1.0-1.2mg initially then 0.6 mg PO daily BID during acute attack. Risk for diarrhea
  • NSAIDs early careful if risk factors – renal insufficiency, GI bleeds
  • Only start allopurinol if >3flares/yr, tophi, joint destruction, renal stones, or tumour lysis syndrome. Continue allopurinol if already on it prior to acute attack
354
Q

Definition of pseudogout?

A

Calcium pyrophosphate dihydrate crystals (CPPD) deposited in cartilage, positive birefringent, rhomboid shape

355
Q

Clinical presentation of pseudogout?

A

Acute arthritis, swelling, pain, erythema, swollen tender joint, can mimic gout but affects large joints

356
Q

Diagnosis of pseudogout?

A
  • Aspiration - rhomboid shaped and +vely birefringent (unlike gout which is needle shaped and –vely bifringent).
  • Radiology: Suspect if chondrocalcinosis on Xray
357
Q

Risk factors of pseudogout?

A

Metabolic (hemochromatosis, hyperparathyroidism, low PO4/Mg, Wilson’s), pre-existing OA, renal failure/dialysis, idiopathic (most common)

358
Q

Treatment of pseudogout?

A

NSAIDs, local steroid injection, rarely oral steroids. RICE (rest, ice, compression, elevation). NOTHING PREVENTS CPPD (unlike Allopurinol in gout)

359
Q

Definition of OA

A

Mechanical joint disease and the most common joint disease

360
Q

Epidemiology of OA

A

F=M <50yo, F>M slightly in >50yo (generalized nodal osteoarthritis in perimenopausal women)

361
Q

Clinical features of OA

A
  • Any time of day, minimal morning stiffness <30mins, worse with activity – improved with rest,
  • Deformity, bony enlargement, crepitus, limitation of movement, peri-articular muscle atrophy
362
Q

Risk factors for primary OA

A

Excess weight, excess wear (due to occupation or sports), genetics (multigenic, 65% heritability, esp. in hands)

363
Q

Risk factors for secondary OA

A

Other joint disorders (rheumatoid arthritis, hemophilia, crystal, congenital dysplasias); injury (traumatic, post surgical); metabolic diseases

364
Q

Distribution of primary OA

A

Hands (DIPs=Heberdan, PIPs=Bouchard; 1st CMCs (thumb squaring), scaphotrapezial joint of wrist), hips, knees, 1st MTPs, cervical and lumbar spine

365
Q

Distribution of secondary OA

A

Atypical sites/presentations (wrists, elbows, shoulders, ankles, MCPs) and young patients

366
Q

Physical exam findings of OA

A
  • Bony enlargement/overgrowth
  • Malalignment in 50% (varus > valgus knee; angulation of fingers)
  • Muscle atrophy (esp. quad mms with knee)
  • Limited ROM active and passive (articular problem), tenderness, crepitus
  • +/- effusion
367
Q

Radiographic findings of OA

A

Joint space narrowing, subchondral sclerosis, subchondral cysts, osteophytes

368
Q

Conservative treatment of OA

A

Patient education, weight loss, low impact exercise, walking aids (canes)

369
Q

Pharmacological treatment of OA

A

1st line: acetaminophen up to 4 g/d (OA is not an inflammatory disorder)
2nd line: NSAIDs (COX-2 selective) in low doses for short durations
3rd line: combination analgesics (e.g. acetaminophen and codeine)
Other pharmacological adjuncts:
- intra-articular corticosteroid or hyaluronic acid injections
- topical NSAIDS (diclofenac)
- capsaicin cream
- oral glucosamine

370
Q

When should surgery be considered for OA?

A

Consider if persistent significant pain and functional impairment despite optimal pharmacotherapy

371
Q

Surgical treatment for OA?

A

Debridement, osteotomy, total joint arthroplasty

372
Q

Red flags of non-articular musculoskeletal pain?

A
  • Recent trauma
  • Pain at rest
  • Pain awakening them at night
  • New medications
  • An immuno-compromised state
  • A history of cancer
  • Constitutional symptoms
  • Vascular or neurological symptoms.
373
Q

Questions to ask on history for non-articular musculoskeletal pain?

A
  • HPI: OPQRST
  • Recent trauma, repetitive strain, infective or constitiutional sx
  • Risk factors for DVT
374
Q

Ddx of localized non-articular musculoskeletal pain <6 weeks?

A
  • Trauma (dislocation or torn tendon)
  • Infections (necrotizing fascitis, cellulitis, or osteomyelitis)
  • Vascular compromise (DVT, compartment syndrome, or sickle cell disease)
375
Q

Ddx of localized non-articular musculoskeletal pain >6 weeks?

A
  • Mechanical strains (bursitis or tendinitis)
  • Vascular disease (peripheral vascular disease or intermittent claudication)
  • Neoplastic
376
Q

Ddx of diffuse non-articular musculoskeletal pain?

A
  • Viral illness
  • Drug reaction
  • Polymyalgia rheumatica (PMR)
  • Fibromyalgia
377
Q

Definition of myofascial pain syndrome?

A

A non-inflammatory disorder of musculoskeletal origin, associated with pain and muscle stiffness, characterized by the presence of hyperirritable palpable nodules in the skeletal muscle fibers, which are termed myofascial trigger points (knots)

378
Q

Diagnosis of myofascial pain syndrome?

A
  • Essential - taut band palpable, spot tenderness of a nodule, painful limit to full stretch
  • Confirmatory – local twitch response, Pain or altered sensation (in expected distribution) on compression of tender nodule, Imaging of a local twitch response induced by needle penetration of a tender nodule.
379
Q

Risk factors of myofascial pain syndrome?

A
  • Ergonomic factors – head, shoulder posture, repetitive activities – more of a mechanical disorder than a neurological one
  • Structural factors – scoliosis (Scoliosis - certain muscles have to compensate and can lead to imbalance and increased risk of MPS), pelvic asymmetry, arthritis of joints, trauma
  • Medical factors
380
Q

Pathophysiology of myofascial pain syndrome?

A

Trauma – taut band (chronically contracted fibres within muscle, with more concentrated areas of contraction in nodules)– latent MTrP (palpable, no symptoms) either goes to spontaneous recovery, active MTrP (palpable, tender and symptoms) or persistence without progression

381
Q

Common sites for myofascial pain syndrome?

A
  • Sternocleidomastoid – might cause referred pain in the forehead, occipital area (therefore could headaches is on differential)
  • Extremities, lower back
382
Q

Treatment for myofascial pain syndrome?

A
  • Active – education, exercise, postural/mechanical/ergonomic modifications. Focus is on active treatments.
  • Passive – pharmacologic (NSAIDs for short-term or flare, TCA, SSRI for chronic pain modulators), trigger point injections – saline, local anesthetic, corticosteroid, botox, CAM therapies (acupuncture, massage)
383
Q

Mechanism of injury for muscle strains

A

Occurs when muscle is elongated passively or activated while being stretched. Eccentric exercise highest. Sudden acceleration or deceleration.

384
Q

Common sites of muscle strains

A

Hamstring (biceps femoris most common) and Quads (rectus femoris most commonly affected) and Gastrocnemius. All cross 2 joints.

385
Q

What is a grade 1 muscle strain

A

Small amount of fibers are stretched – pain but usually full strength, not much swelling. Muscle is very vascular so when you have significant muscle injury, there is bruising and swelling

386
Q

What is a grade 2 muscle strain

A

Partial tear – pain, swelling and weakness. Most of them are actually across the whole muscle area but there still is continuity remaining across the tear

387
Q

What is a grade 3 muscle strain

A

Complete tear, usually occurs at the musculotendinous junction. Pain, swelling, loss of function. If you’re tight, especially when you’re growing, muscles elongate but tendons stay tight

388
Q

Treatment of muscle strain

A

RICE – rest, ice, compression, elevation. Short term NSAIDS. Worsens if exercise resumed prematurely even though exercise decreases symptoms. If in hamstring, takes 6-9months to recover.

389
Q

Contributing factors of muscle strain

A

Inadequate warm-up, muscle imbalance, excessive muscle tightness, insufficient joint ROM, inadequate recovery

390
Q

Mechanism of injury of muscle contusion

A

Direct blow to a muscle “charley horse”. Bleeding from muscle damage

391
Q

Mechanism of injury of tendon ruptures

A

Sudden loading of the musculotendinous unit (usually in older people) can cause this as can weak/poorly vascularized tendons from a history of tendonitis. As tendons get further away from muscle, they have less blood supply and this makes them vulnerable as we age or with repeated injuries.

392
Q

Complications of muscle contusion

A

Trying to avoid compartment syndrome and myositis ossificans – occurs when a hematoma calcifies. Consider when not improving or devastating stiffness or shortening of muscle. If it happens posteriorly, there are some neurovascular complications that can occur

393
Q

Treatment of muscle contusion

A

PRICE, codeine, followed by gentle ROM and strengthening. NSAID use can decrease platelets early on and this can cause more bleeding. Heat can also cause more bleeding.

394
Q

Mechanism of injury for biceps brachialis ruptures?

A

Proximal (lifting weights) or distal (sudden loading).

395
Q

Clinical presentation of proximal biceps brachialis rupture

A

Proximal pain, tenderness, bunching up of muscle belly, weak ARM flexion (not much elbow flexion) and supination. So people don’t have much dysfunction with elbow flexion but you can break their supination

396
Q

Clinical presentation of distal biceps brachialis rupture

A

Distal pain, tenderness, palpable defect, weak supination. Hook test – can’t hook tendon with index finger. Usually the next day they get significant bruising and swelling and it becomes more obvious

397
Q

Treatment of proximal biceps brachialis rupture

A

Treat conservatively with physio. Only need surgery if professional athlete

398
Q

Treatment of distal biceps brachialis rupture

A

Treat OPERATIVELY – up to 50% loss of flexion/supination strength with cons. All biceps muscles have a common insertion distally so NEEDS repair

399
Q

Mechanism of injury for knee extensor rupture?

A

Sudden forceful contraction of quadriceps during an attempt to stop

400
Q

Risk factors for knee extensor rupture?

A

More common in obese patients and those with pre-existing degenerative changes in tendon - DM, SLE, RA, steroid use, renal failure on dialysis

401
Q

Clinical features of knee extensor rupture?

A
  • Inability to extend knee or weight-bear
  • Possible audible “pop”
  • Patella in lower or higher position with palpable gap above or below patella, respectively
  • May have an effusion
402
Q

Investigations for knee extensor rupture?

A
  • Straight Leg Raise – unable to with complete rupture
  • Knee X-ray to rule out patellar fracture, MRI to distinguish between complete and partial tears
  • Lateral view: patella alta with patella tendon rupture, patella baja (infera) with quadriceps tendon rupture
403
Q

Non-operative indications for knee extensor rupture?

A

Incomplete tears with preserved extension of knee

404
Q

Operative indications for knee extensor rupture?

A

Complete ruptures with loss of extensor mechanism

405
Q

Operative treatment for knee extensor rupture?

A
  • Early surgical repair: better outcomes compared with delayed repair - Begin active knee flexion, passive extension 2 weeks post op. Physio start @ 6wks usually
  • Delayed repair complicated by quadriceps contracture, patella migration, and adhesions
406
Q

Non-operative treatment for knee extensor rupture?

A

Immobilization in brace

407
Q

Mechanism of injury of achilles tendon rupture

A
  • Loading activity, stop-and-go sports (e.g.squash, tennis, basketball)
  • Secondary to chronic tendonitis, steroid injection
408
Q

Clinical features of achilles tendon rupture

A
  • Audible pop, sudden pain with push-off movement
  • Pain or inability to plantar flex
  • Palpable gap
  • Apprehensive toe off when walking
  • Weak plantar flexion strength
  • Thompson test: with patient prone, squeeze calf, normal response is plantar flexion. No passive plantarflexion is positive test = ruptured tendon
409
Q

Investigations for achilles tendon rupture

A

X-ray (to rule out other pathology), U/S or MRI (for partial vs. complete ruptures)

410
Q

Non-operative indication for achilles tendon rupture

A

Low athletic demand (new level 1 evidence suggests no difference in re-rupture rates between operative and non-operative management with functional rehabilitation)

411
Q

Non-operative treatment for achilles tendon rupture

A

Initial cast foot in plantar flexion (to relax tendon), with functional rehabilitation x 8-12 wk

412
Q

Operative treatment for achilles tendon rupture

A

Surgical repair, followed by functional rehabilitation x 8-12 wk

413
Q

Operative indication for achilles tendon rupture

A

High athletic demand

414
Q

Mechanism of injury of tendonitis

A

Thought to be from a repetitive mechanical load with a subsequent inflammatory response. Histopathological studies in the 1990s showed more degenerative tendon changes rather than inflammation.

415
Q

Clinical presentation of tendonitis

A
  • Pain, stiffness, and crepitus with ROM
  • Thickened tendon, palpable bump
  • More frequently the morning after exercise, with use
416
Q

Treatment of tendonitis

A
  • Rest, NSAIDs, shoe wear modification (orthotics, open back shoes)
  • Heel sleeves and pads are mainstay of non-operative treatment
  • Gentle gastrocnemius-soleus stretching, eccentric training with physical therapy, deep tissue calf massage
  • Shockwave therapy in chronic tendonitis
  • Do not inject steroids (risk of tendon rupture)
417
Q

Definition of plantar fasciitis?

A
  • Inflammation of plantar aponeurosis at calcaneal origin

- Common in athletes (especially runners, dancers)

418
Q

What is plantar fasciitis associated with?

A

Associated with obesity, DM, seronegative and seropositive arthritis

419
Q

Mechanism of injury of plantar fasciitis

A

Repetitive strain injury causing microtears and inflammation of plantar fascia

420
Q

Clinical features of plantar fasciitis

A
  • Insidious onset of heel pain, pain when getting out of bed, and stiffness
  • Intense pain when walking from rest that subsides as patient continues to walk, worse at end of day with prolonged standing
  • Swelling, tenderness over sole
  • Greatest at medial calcaneal tubercle and 1-2 cm distal along plantar fascia
  • Pain with toe dorsiflexion (stretches fascia)
421
Q

Investigations for plantar fasciitis

A
  • Plain radiographs to rule out fractures
  • Often see bony exostoses (heel spurs) at insertion of fascia into medial calcaneal tubercle
  • Spur is secondary to inflammation, not the cause of pain
422
Q

Definition of ligament injury

A

Ligaments increase the stability of a joint. Load is transferred in the direction of the ligaments from bone to bone. Injuries occur when a ligament is under excessive load

423
Q

What is grade 1 ligament injury

A

Mild sprain, few fibres torn, stretching of the ATFL. Clinically, ligament is stable (no laxity) with solid endpoint

424
Q

What is grade 2 ligament injury

A

Moderate sprain, incomplete tear. Clinically, swelling is present and there is increased laxity with an end point

425
Q

Non-operative treatment of plantar fasciitis

A
  • pain control and stretching programs are first-line
  • rest, ice, NSAIDs, steroid injection
  • physiotherapy: Achilles tendon and plantar fascia stretching, extracorporeal shockwave therapy
  • orthotics with heel cup - to counteract pronation and disperse heel strike forces
426
Q

Operative treatment of plantar fasciitis

A
  • very rarely indicated

- when performed, includes endoscopic release of fascia

427
Q

What is grade 3 ligament injury

A

Severe sprain with complete tear. Grade 3 injuries can have less pain as sensory fibers are completely divided.

428
Q

Investigations for ligament injury

A

X-Ray (check for bony injury – Ottawa Ankle Rules), MRI (usually not needed unless not improving)

429
Q

Treatment for ligament injury

A

Restore stability to joint. Grade 1 + 2 = physio and brace and RICE (rest, ice, compression, elevation) but Grade 3 = usually conservative but may brace or do surgery.

430
Q

Etiology of bursitis?

A
  • Overuse injuries in the bursa are common
  • Excessive shearing or compressive forces
  • Traumatic
431
Q

Common areas of bursitis?

A

Subacromial bursa, greater trochanteric bursa, prepatellar bursitis, Iliotibial band friction syndrome

432
Q

Treatment of bursitis?

A
  • Removal of irritating loads, lengthening, strengthening
  • Reduction of inflammation - PRICE, NSAIDs
  • Corticosteroid injections – under ultrasound guidance
  • Traumatic – pre-patellar - aspiration and compression to avoid increased swelling