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MSK > Lecture 3: Misc MSK Injuries > Flashcards

Lecture 3: Misc MSK Injuries Flashcards

1
Q

Essentials of diagnosis of Osteomyelitis

A
  • Fever with bone pain and tenderness
  • positive blood cultures
  • Elevated ESR/CRP
  • Early radiographs are typically negative, esp within 2 weeks

Trending ESR and CRP is much better than WBC due to chronicity

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2
Q

What are the causes of osteomyelitis?

A
  • Hematogenous spread
  • Contiguous spread
  • Secondary infection d/t vascular insufficiency or neuropathy
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3
Q

Who is hematogenous osteomyelitis MC in? Where exactly?

A

Children, esp males, in their metaphysis in long bones

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4
Q

MC primary site of hematogenous osteomyelitis?

A

Urinary tract, skin/soft tissue, IV sites, endocardium, dentition

Staph

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5
Q

where is hematogenous spread MC in adults

A

vertebral column LS>TS>CS

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6
Q

Biggest RFs for hematogenous osteomyelitis in adults

A
  • IVDU
  • Diabetes
  • IVs

in children - sickle cell, comp delivery, maternal infections, premature

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7
Q

Who is contiguous spread osteomyelitis MC in and how?

A

Adults, usually post fracture/open wound (diabetic ulcers)

Most commonly polymicrobial

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8
Q

How does osteomyelitis present?(4)

A
  • Gradual onset of S/S
  • Dull pain at site, fever and rigors
  • Tenderness, warmth, erythema, swelling on exam
  • Probing for bone is recommended if ulcer is present
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9
Q

How does vertebral involvement of osteomyelitis present?(4)

A
  • Much slower onset
  • Localized pain/tenderness
  • Pain with percussion over affected area
  • Neurologic symptoms in 1/3 of pts
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10
Q

Dx of osteomyelitis

A
  • Early XR: maybe swelling, loss of tissue planes, periarticular demineralization of bones
  • Later XR: Periosteal thickening or elevation, bone cortex irregularity
  • Ideal: CT or MRI, which is highly sensitive
Moth eaten

Children: 5-7d for changes
Adults: 10-14d for changes

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11
Q

When is CT/MRI indicated for osteomyelitis evaluation?

A
  • Onset < 2 weeks at presentation
  • XR neg but clinical presentation is suspicious
  • positive neuro findings on exam

MRI is especially good for feet

Nuclear is alternative.

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12
Q

Who is bone biopsy indicated in for osteomyelitis?

A

Any patient with radiologic evidence without + blood cultures.

Do not delay biopsy due to abx use.

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13
Q

What would histology show for a positive bone biopsy for osteomyelitis?

A

Necrotic bone with extensive resorption adjacent to an inflammatory exudate

Must collect through an uninfected site if percutaneous.

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14
Q

Empiric ABX for osteomyelitis

A

MRSA and G- coverage: Vanco +3/4th gen cephalosporin

Typically only used in long-bone infections

ceftriaxone, ceftaz, cefepime

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15
Q

How long is staph osteomyelitis? what is the abx regimen used for this strain?

A

4 weeks

  • IV cefazolin, nafcillin or oxacillin
  • MRSA = vanc
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16
Q

If you want to transition a pt to PO abx for osteomyelitis, what is the combo?

A

After 2 weeks of IV agents at minimum, you can use Levofloxacin/ciprofloxacin + rifampin

can also use bactrim, doxy, or clinda

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17
Q

When is debridement indicated for osteomyelitis?

A
  • Infection related to open fx or surgical hardware
  • Extensive diseas involving multiple bony/ soft tissue layers
  • Concomitant joint infection
  • Recurrent/persistent infection
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18
Q

Persistent elevation of what labs over 2 weeks with appropriate ABX is suggestive of a persistent osteomyelitis infection?

A

ESR/CRP

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19
Q

What are the complications of osteomyelitis?

A
  • Pathological fx
  • Chronic
  • Impaired bone growth
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20
Q

What is chronic osteomyelitis?

A

Bone infection over months-years resulting in the development of a sequestrum +/- sinus tract

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21
Q

what bone changes occur in chronic osteomyelitis

A
  • increased intramedullary pressure causes rupture of periosteum and formation of cloaca (sinus tract)
  • periosteal blood supply interruptions lead to necrosis
  • necrotic bone leads to sequestrum
  • new bone forms in areas where periosteum was damaged (involucrum)
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22
Q

What is involucrum?

A

Bone formation in areas where the periosteum was damaged

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23
Q

Where is chronic osteomyelitis MC in?

A
  • Sternal
  • Mandibular
  • Feet
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24
Q

How does chronic osteomyelitis present?

A
  • Pain, erythema, swelling
  • +/- draining sinus tract
  • fever usually not present
  • bone palpation is positive
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25
Q

How do labs differ between chronic vs acute osteomyelitis?

A

Leukocytosis and ESR/CRP are rarely elevated in chronic.

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26
Q

What is a marjolin ulcer?

A

Epithelium of the sinus tract develops squamous cell carcinoma

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27
Q

Management of chronic osteomyelitis

A
  • Debridement
  • Obliteration of dead space
  • Long-term ABX therapy
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28
Q

What is compartment syndrome?

A

Increased pressure within a limited space compromises the circulation and function of the muscles and nerves within that space

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29
Q

What are the 4 compartments of the lower leg?

A
  1. Anterior
  2. Lateral
  3. Superficial posterior
  4. Deep posterior

MC location for compartment is lower leg

30
Q

What is normal compartment pressure and how long can we tolerate increased pressure?

A
  • 10mm is normal, but we can tolerate up to 20 without damage.
  • After around 8h, we start developing neuropathy.
  • After around 12h, myocytes die and we develop contractures
31
Q

Clinical presentation of compartment syndrome?

A
  • Pain out of proportion
  • Pain that worsens with passive stretching
  • Paresthesias within 30min onset
  • Tense to palpation
  • Decreased sensation (use 2 point)
  • Weak pulse in severe

Paralysis is late and pallor is rare

32
Q

How do you measure compartment pressure?

A
  • Two separate measurements within 5 cm of the site
  • Pressures must be > 45 mm/Hg
  • Must account for hypotensive patients, aka if DBP is within 30 of their compartment pressure. (DBP of 52 with pressure of 28 = compartment syndrome)

DO NOT USE in hands or feet

33
Q

Management of compartment syndrome?

A
  1. Remove casts/dressings
  2. Elevate affected limb
  3. Surgical fasciotomy if patient has had it within 24h-48h
34
Q

Essentials of rhabdomyolysis

A
  • Crush injuries
  • Serum elevations in CK and lyte abnormalities
  • Release of myoglobin leads to renal toxicity
35
Q

What is rhabdomyolysis?

A
  • Acute skeletal muscle cell death leading to release of intracellular contents
  • ATN will occur, leading to AKI
36
Q

What causes ATN due to rhabdo?

A

Hypovolemia + myoglobin + uric acid crystals + decreased GFR + nephrotoxic ferrihemate (metabolite of myoglobin)

37
Q

Clinical presentation of rhabdomyolysis

A
  • Dark tea colored urine
  • Myalgias and weakness
  • Malaise, low-grade fever
  • N/V, abd pain, and tachy if severe

Similar to a flu patient

swelling/tender of involved muscles. AMS d/t severe renal failure and urea-induced encephalopathy if severe!

38
Q

Dx of rhabdo

A
  • Elevated CK 5x ULN(Most sensitive)
  • UA showing tea color when urine myoglobin is > 100
  • A + blood on UA with negative RBC on microscopy = myoglobinuria
  • CMP: Elevated phosphorus, uric acid, BUN/Cr, AST/ALT, K+. low calcium.
  • CBC to monitor potential DIC

A UA cant differentiate blood and myoglobin

can see cardiac dysrhythmias on EKG d/t hyperkalemia or hypocalcemia

39
Q

Management of Rhabdo

A
  • IVF aggressively for first 72h early
  • Monitor I&O to get goal of 200-300 urine output
  • Urine alkalization via bicarb only if CK levels are higher than 5000, acidemia, dehydration or underlying renal disease
40
Q

When would you treat hypocalcemia in rhabo?

A

Only if hyperkalemia is present

41
Q

Discharge criteria for rhabdo

A
  • Normal renal
  • Normal lytes
  • Alkaline urine
  • Isolated cause of injury
  • No uncontrolled comorbidities
42
Q

Main complications of rhabdo

A
  • AKI
  • Compartment syndrome
  • DIC
43
Q

What is fibromyalgia?

A

Chronic condition characterized by multiple MSK pain with multiple tender points but no objective findings

44
Q

MC demographic for fibromyalgia

A

20-55

45
Q

Presentation of Fibromyalgia

A
  • Chronic fatigue and generalized aching pain
  • Depression
  • Widespread soft tissue tenderness
  • No joint involvement
46
Q

How is fibromyalgia diagnosed?

A

ACR criteria:

  1. Widespread pain index (WPI) > 7 + symptom severity (SS) > 5 or WPI 3-6 with SS > 9
  2. 3months
  3. No other disorder

Dx of exclusion

47
Q

Management of fibromyalgia

A
  • Patient education
  • CBT
  • Exercise
  • Wt loss if overweight
  • Muscle relaxant: flexeril
  • Antidepressants
  • Neurontin/pregabalin
  • Tramadol

Careful of tramadol addiction

48
Q

Treatment protocol for fibromyalgia

A

**On average: start with cyclobenazeprine and amitriptyline QHS

49
Q

What is neurogenic arthropathy/charcot joint?

A

Condition characterized by progressive destruction of bone and soft issues at weight bearing joints

50
Q

What is the hallmark sign of neurogenic arthropathy?

A

Mid-foot collapse, described as a rocker-bottom foot

51
Q

MC etiologies for neurogenic arthropathy

A
  • DM (MC)
  • Cerebral palsy
  • Alcoholic neuropathy
  • Spinal cord injury
  • Syphilis
52
Q

Where does neurogenic arthropathy occur most commonly?

A
  • Foot
  • Ankle
  • Tarsometatarsal joint
  • Ankle articulations

articulations are cuneonavicular, talonavicular and calcaneocuboid articulations

53
Q

Presentation of neurogenic arthropathy

A
  • Unilateral warmth, redness, and edema oer joint
  • Hx of minor trauma
  • Pain is present but low severity
  • Loss of arch, bony protrusions
  • 40% have concomitant ulcers
54
Q

Dx imaging of neurogenic arthropathy

A
  • XR with weight-bearing
  • MRI if XR negative OR osteomyelitis is in DDx
55
Q

What 3 things are key to look at for an XR for neurogenic arthropathy?

A
  • Progressive decline of the yellow angle (calcaneal inclination)
  • Equinus deformity (can’t dorsiflex)
  • Destruction of TMT joint (red line)
56
Q

Staging of neurogenic arthropathy

A
  1. Stage 0: early/inflammatory - localized swelling, erythema, warmth. little/no xray findings
  2. Stage 1: cont localized inflamm. Xray - fx, subluxation/dislocation, bony debris.
  3. Stage 2: coalescence with decreasing inflammation and healing of XR findings
  4. Stage 3: Remodeling with no inflammation, bony deformities, and mature fracture callus.
57
Q

Tx for stage 0-2 neurogenic arthropathy

A
  • Avoid weight-bearing via casting of foot
  • CROW (charcot restraint orthotic walker) use
58
Q

Tx for stage 3 or failed therapy neurogenic arthropathy

A

Discuss risk/benefit of surgery

59
Q

What is Raynaud’s phenomenon?

A
  • Syndrome of paroxysmal digital ischemia in cold or emotional stress.
  • Vasoconstriction and then rapid vasodilation

MC in the fingers

60
Q

What is primary Raynaud’s?

A
  • NO vascular structural abnormalities
  • MC in healthy females 15-30
  • FMHx

MC type

61
Q

What is secondary Raynaud’s?

A
  • Underyling systemic condition leads to Raynaud’s
  • MC in males > 40
  • MC with rheumatologic conditions
  • Frostbite, jackhammers
  • More severe and higher risk of ulceration/gangrene
62
Q

What are raynaud attacks?

A
  • Sudden onset of cold digits with demaracation of skin pallor (white attack) or cyanosis (blue attack)
  • Massive erythema when rewarming
  • MC in the index, middle, and ring fingers
Sclerodactylyl, calcinosis
63
Q

What do nailfold capillaries look like in raynaud’s?

A
64
Q

Management of primary raynaud’s

Normal PE and nailfold capillaries

A
  • Pt Ed
  • Regular f/u
65
Q

Management of secondary raynaud’s

A

Tx underlying

66
Q

What is the patient education for Raynaud’s?

A
  • Mittens and stockings
  • Avoid vasoconstrictors
  • Smoking cessation
67
Q

First-line pharmacologic therapy for Raynaud’s

A
  1. CCBs (amlodipine)
  2. NTG or PDE5 inhibitors

Indicated if failure to control symptoms

If all fails, refer to vascular

68
Q

What is Marfan’s syndrome?

A

Genetic disorder of CT tissue characterized by skeletal, ocular, and CV abnormalities

1 in 5000

69
Q

Presentation of Marfan’s

A
  • Tall, long arms, and digits (arachnodactylyl)
  • Scoliosis
  • Pectus Carinatum/excavatum
  • Ecotopia lentis (eye lens displacement)
  • Myopia (Near sighted)
  • Retinal detachment
  • MVP
  • Aortic root dilation => aortic regurg or dissection
70
Q

How is marfan’s confirmed?

A

Genetic testing showing a mutation in the fibrillin gene (FBN1) on chromosome 15

71
Q

What criteria is used to score marfan syndrome?

A

Ghent criteria

No need to memorize criteria components

72
Q

How do we manage Marfans?

A
  • Annual Ophthalmology
  • Annual Orthopedic
  • Annual Echo/cardio
  • Long term BBs (atenolol/metoprolol)
  • Restriction from vigorous physical exertion

MSK (27 decks)

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