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MSK > Misc Disorders > Flashcards

Misc Disorders Flashcards

1
Q

What is osteomyelitis?

A

Infection of bone and inflammation of fatty tissues

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2
Q

Essentials of osteomyelitis diagnosis

A
  • Fever associated with bone pain and tenderness
  • Microbiologic diagnosis often made from blood cultures
  • Elevated ESR and CRP common
  • Early radiographs typically negative
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3
Q

Cause of osteomyelitis

A
  • Hematogenous spread
  • Spread from contiguous site of infection/open wound
  • Secondary infection in setting of vascular insufficiency or concomitant neuropathy
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4
Q

Duration of osteomyelitis

A
  • Acute
  • Chronic
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5
Q

Pathophysiology of hematogenous spread

A
  • Typically due to bacteremia and begins in medullary canal
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6
Q

Epidemiology of hematogenous spread

A
  • Most common in children
  • Male
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7
Q

Where is osteomyelitis due to hematogenous spread most commonly seen in children?

A
  • Metaphysis of long bones
  • Hemoglobinopathies such as sickle cell increase risk
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8
Q

Risk factors for hematogenous spread of osteomyelitis in children

A
  • Complicated delivery
  • Maternal infection at delivery
  • Prematurity
  • Indwelling catheters
  • Urinary tract anomalies
  • Sickle cell
  • Immunodeficiency disorders
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9
Q

MC primary site of infections cause osteomyelitis through hematogenous spread

A
  • Urinary tract
  • Skin/soft tissue
  • Intravascular catheterization sites
  • Endocardium
  • Dentition
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10
Q

MC organisms in children leading to osteomyelitis through hematogenous spread

A
  • S. aureus (MC)
  • Salmonella (sickle cell)
  • Group A and B strep
  • Strep. pneumo
  • E. Coli
  • Kingella Kingae (other countries)
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11
Q

Where does osteomyelitis often manifest in adults through hematogenous spread?

A

Vertebral column (LS > TS > CS)

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12
Q

Risk factors for osteomyelitis due to hematogenous spread in adults

A
  • Age
  • IVDU
  • Diabetes
  • IVs
  • Indwelling urinary catheters
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13
Q

MC organisms in adults causing hematogenous spread leading to osteomyelitis

A
  • S. aureus (MC)
  • Pseudomonas (IVDU)
  • Gram - organisms (elderly)
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14
Q

What is contiguous spread?

A

Infection traveling from a soft tissue site

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15
Q

Causes of contiguous spread leading to osteomyelitis

A
  • Open fractures/trauma
  • Prosthetic devices
  • Neurosurgery
  • Septic arthritis
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16
Q

Pathophysiology of contiguous spread of osteomyelitis

A
  • Symptoms begin 1 month after inoculation
  • Infection inoculates the bony cortex and migrates towards the medullary canal
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17
Q

Who is most at risk for osteomyelitis due to contiguous spread?

A

Adults

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18
Q

MC organisms causing contiguous spread of osteomyelitis

A
  • S. aureus
  • Staph epidermidis
  • Streptococcus
  • Polymicrobial infections more common for contiguous spread
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19
Q

What causes secondary osteomyelitis due to comorbid conditions?

A
  • Chronic, progressive soft tissue infection of foot or ankle
  • Hip and sacrum can be involved
  • Most often related to diabetes/diabetic ulcers and vascular insufficiency
  • Polymicrobial infections common: s. aureus and B-hemolytic strep MC
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20
Q

Clinical presentation of osteomyelitis

A
  • Gradual onset of symptoms over several days - weeks
  • Dull pain at involved site
  • +/- worse with movement
  • Fever and rigors
  • Tenderness
  • Warmth
  • Erythema
  • Swelling on exam
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21
Q

What should be done in osteomyelitis if ulcer present?

A

Probing for bone

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22
Q

What is the presentation of vertebral involvement of osteomyelitis?

A
  • Slower progression –> 3 weeks - 3 months
  • Localized pain and tenderness of involved vertebrae
  • Often more than one vertebrae involved including intervertebral disks
  • Pain increased with percussion over affected area
    • fever in 1/2 of patients
  • +/- neurologic symptoms (due to extension of infection leading to spinal epidural abscess)
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23
Q

Presentations of osteomyelitis in nonverbal patients/pediatrics

A
  • Decreased use/movement
  • Fussiness
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24
Q

Presentations of hip, pelvis, vertebral involvement of osteomyelitis?

A

Predominantly pain with few other symptoms

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25
Q

Diagnostics for osteomyelitis

A
  • Organism isolation in bone, blood, or contiguous focus: blood cultures + in 60% of cases (cultures from wounds, ulcers not reliable)
  • CBC: elevated WBC - left shift in acute infection
  • ESR and CRP - elevated: helpful to monitor throughout treatment course
  • BMP: assess renal and livery function before starting pharmacotherapeutics
  • XRAY
  • CT/MRI
  • Nuclear studies: if MRI contraindicated
  • Bone biopsy: if radiologic evidence without + blood cultures
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26
Q

Findings of early osteomyelitis on xray

A
  • Abnormal findings may not be present early in course –> children 5-7 days + and adults 10-14 days +
  • Possible soft tissue swelling
  • Loss of tissue planes
  • Periarticular demineralization of bone
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27
Q

Findings of late osteomyelitis on XRAY

2 weeks after symptoms

A
  • Periosteal thickening or elevation
  • Bone cortex irregularity: osteolysis, endosteal scalloping, regional osteopenia
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28
Q

Findings of chronic osteomyelitis on xray

A
  • New bone formation
  • Sclerosis
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29
Q

This test for osteomyelitis is highly sensitive and specific, preferred for foot infections

A

MRI/CT

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30
Q

What are indications for CT/MRI of osteomyelitis

A
  • Onset <2 weeks at presentation
  • X-ray is negative in a clinical presentation consistent with infection
    • neurologic findings on exam
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31
Q

When would MRI be avoided in osteomyelitis

A
  • Indwelling metal devices
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32
Q

When might an ultrasound be considered in osteomyelitis?

A

Considered in early cases
Identify joint effusions and extra-articular soft tissue fluid infections

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33
Q

When would a nuclear study be performed?

A

If MRI is contraindicated
High sensitivity but low specificity

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34
Q

Indications for bone biopsy in osteomyelitis?

A
  • All patients with radiologic evidence of osteomyelitis without + blood cultures
  • Osteomyelitis by hematogenous spread doesn’t require bone bx
  • Do not delay due to abx use
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35
Q

Technique for bone biopsy

A
  • Open –> can be during debridement
  • Percutaneous biopsy –> often image (CT) guided, needed for vertebral osteomyelitis and must be collected through uninfected soft tissue
  • Assess biopsy specimen for gram stain, C&S, and histology
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36
Q

What does histology of osteomyelitis show?

A

Necrotic bone with extensive resorption adjacent to an inflammatory exudate

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37
Q

How is osteomyelitis managed?

A
  • Consult ID and ortho
  • Empiric antibiotics in long bone infections covering MRSA and gram - organisms
  • Vancomycin + 3rd or 4th gen cephalosporin (ceftazidime, ceftriaxone, cefepime)
  • Tailor ABX therapy to culture and susceptibility data once available
  • Hardware removal if not needed for bone stability or location affects debridement
  • Debridement
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38
Q

What type of antibiotic therapy is preferred?

A
  • IV during acute phase of infection, especially if signs of systemic toxicity
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39
Q

How long should staphylococcal osteomyelitis be treated?

A

At least 4 weeks

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40
Q

What is treatment for methicillin-sensitive osteomyelitis?

A
  • IV cefazolin
  • Nafcillin
  • Oxacillin
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41
Q

What is treatment for methicillin-resistant staphy

A

Vancomycin with goal trough level of 15-20 mcg/mL

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42
Q

What can be done if S. aureus isolates in osteomyelitis show susceptibility to oral agents?

A

Combo therapy for 4-6 weeks following 2 weeks of administration of appropriate IV agents
* Levofloxacin or ciprofloxacin + rifamprin best
* Trimethoprim-sulfamethoxazole, doxycycline, or clindamycin could be considered

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43
Q

What is debridement?

A

Removal of necrotic material and culture of involved tissue and bone

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44
Q

Indications for debridement in osteomyelitis

A
  • Infection related to open fracture or surgical hardware
  • Extensive disease involving multiple bony and soft tissue layers
  • Vertebral osteomyelitis, subperiosteal collection, abscess, or necrotic bone present
  • Presence of concomitant joint infection
  • Recurrent or persistent infection despite standard medical therapy
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45
Q

If therapy for osteomyelitis is prolonged what should be done?

A
  • Antimicrobial monitoring via labs
  • Serial exams until complete resolution
  • Serial radiographic imaging not recommended d/t persistent inflammatory changes that can be mistaken for persistent infection
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46
Q

What is IV antimicrobial monitoring?

A
  • CBC and CMP weekly
  • ESR and CRP at beginning and end of IV therapy and any time symptoms worsen
  • If ESR/CRP remains elevated 2 weeks after completion of abx therapy consider persistence of osteomyelitis
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47
Q

What is PO therapy osteomyelitis monitoring?

A
  • CBC
  • Cr and ALT at 2, 4, 8, 12 weeks and every 6-12 months after initiation of PO therapy
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48
Q

Complications of osteomyelitis

A
  • Bone destruction leading to pathological fractures
  • Chronic osteomyelitis
  • Impaired bone growth in children: increased risk if growth plate is affected
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49
Q

What is chronic osteomyelitis?

A
  • Long-standing bone infection over months or years resulting in development of sequestrum with or without a sinus tract
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50
Q

What are bone changes with chronic osteomyelitis?

A
  • Increased intramedullary pressure leads to rupture of periosteum, which forms a cloaca or sinus tract
  • Periosteal blood supply interruptions leading to necrosis
  • This dead bone can lead to a radiographic finding known as a sequestrum
  • New bone begins to form in areas where the periosteum was damaged, called involcrum
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51
Q

Where is chronic osteomyelitis MC?

A
  • Sternal
  • Mandibular
  • Foot infections
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52
Q

What is the presentation of chronic osteomyelitis?

A
  • Difficulty with weight-bearing and loss of normal function
  • Pain
  • Erythema
  • Swelling may be present
  • +/- draining sinus tract
  • Fever usually not present
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53
Q

All diabetic ulcers should be ….

A

Probed
* Osteomyelitis will likely develop before exposed bone is present
* Palpating bone is suggestive of osteomyelitis

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54
Q

Work up for chronic osteomyelitis

A
  • Same as acute osteomyelitis (will add this later)
  • +/- elevation of ESR/CRP
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55
Q

Management of chronic osteomyelitis

A
  • Surgical debridement
  • Obliteration of dead space (to stabilize the bone)
  • Long-term antibiotic therapy
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56
Q

Complications of chronic osteomyelitis

A
  • Osteolysis and pathologic fractures
  • Rarely, chronic osteomyelitis sinus will undergo metaplasia and develop squamous cell carcinoma
57
Q

What is compartment syndrome?

A
  • Increased pressure within a limited space
  • Compromises circulation and function of muscles and nerves within space
58
Q

Anatomy of compartment syndrome

A
  • Borders of compartment comprised of bone or soft tissue with minimal elasticity
59
Q

What is the most common location of compartment syndrome?

A

Lower leg compartments
4 compartments: anterior, lateral, superficial posterior, and deep posterior

60
Q

In addition to the leg, which other compartments can have compartment syndrome?

A
  • Thigh
  • Upper arm
  • Forearm
  • Hand
  • Foot
61
Q

Pathophysiology of compartment syndrome

A
  • Normal compartment is 10 mmHg
  • Pressures up to 20 mmHg can be tolerated without damage
  • Muscles and nerves most at risk for cell death from ischemia
  • Ischemia occurs after 8 hours leading to neuropathy
  • > 12 hours leads to myocyte death
62
Q

What are causes of compartment syndrome?

A

Increased volume within compartment
* Crush injury
* Fracture
* Reperfusion injury, post-thrombolytic therapy
* Arterial injury
* Insect bite/snake bite
* Iatrogenic
* Prolonged tetanic contractions
* Bleeding disorder
* Phlebitis
* Thromboembolism
* Drug abuse

Prevention of expansion
* Tourniquet
* Burns
* Constrictive dressings
* Casts
* Extravasation of infusions

63
Q

Clinical presentation of compartment syndrome

A
  • Pain out of proportion to the injury/PE findings ***early and sensitive sign
  • Burning, deep and aching
  • Worse with passive stretching of involved muscle
  • Paresthesias within 30-120 minutes of onset
  • Muscle compartment tense to palpation
  • Muscle weakness within 2-4 hours of onset
  • Decreased sensation: 2 point discrimination most reliable early test
  • Paralysis (late finding)
  • Pallor (uncommon)
  • Weak pulse (ony in severe vascular compression

5 Ps: pain, pulse, pallor, paresthesia, paralysis

64
Q

Diagnostics for compartment syndrome?

A
  • Measure compartment pressure
  • Laboratory testing not needed to make the diagnosis but may be needed to evaluate the underlying condition
65
Q

How is compartment pressure measured?

A
  • Avoid in compartments of the hands and feet due to small size of these compartments
  • 2 separate pressure readings should be obtained within 5 cm of the site
66
Q

How is compartment pressure interpreted?

A
  • > 45 mmHg require decompression
  • Difference between DBP and compartment pressure <30 mmHg = inadequate perfusion, decompression needed
67
Q

Steps to determining compartment pressure

A
  • Connect manometer between the syringe and the needle
  • Insert needle into the compartment
  • Inject a few drops of saline to ensure that there are no air pockets and that the needle is not inserted into a tendon
  • The gauge gives pressure reading in mmHg
  • Check pressures twice in each compartment (within 5 mm of fracture site)
  • Also check adjacent compartment pressures because pressures are highest near the injured area

actually typed this out and don’t need to memorize but here it is

68
Q

Management of compartment syndrome

A
  • Remove restrictive casts or dressings if applicable
  • Elevate affected limb
  • Consult surgery for surgical fasciotomy
  • Initially leave wounds open to allow for swelling to subside post fasciotomy
  • After 48-72 hours consider debridement and closure
  • Occasionally delayed closure at 7-10 days may be needed
  • Consult plastics for skin grafting if needed prior to closure
69
Q

Contraindications to surgical fasciotomy

A

Missed timely diagnosis (elevated tissue pressures >24-48 hours)

70
Q

Disposition of compartment syndrome

A
  • Admit all patients with compartment syndrome
  • Those who do not meet indication for fasciotomy perform serial exams to monitor for worsening symptoms
71
Q

Prognosis of compartment syndrome

A
  • Depends on time of diagnosis and intervention
  • Within 6 hours –> most patients will have complete recovery
  • Within 12 hours –> a little over 1/2 of patients will regain normal limb function
  • After 12 hours –> <10% will regain function
72
Q

Essentials of diagnosis of rhabdomyolysis

A
  • Associated with crush injuries to muscle, immobility, drug toxicities, and hypothermia
  • Serum elevations in muscle enzymes (CK) and marked electrolyte abnormalities characteristic
  • Release of myoglobin leads to direct renal toxicity
73
Q

What is rhabdomyolysis

A
  • Acute skeletal muscle death leading to release of intracellular contents: myoglobin, creatine kinase, purine, AST, ALT, K+, PO43-
  • Leads to acute tubular necrosis resulting in acute kidney injury in 30-40% of patients
74
Q

What does acute tubular necrosis result from?

A

Hypovolemia and combination of the following:
* Precipitation of myoglobin and uric acid crystals within renal tubules (uric acid is a metabolite of purine which is released from injured muscles)
* Decreased glomerular perfusion due to hypovolemia from third spacing due to influx of extracellular fluid into injured muscles
* Nephrotoxic effect of ferrihemate (metabolite of myoglobin)

75
Q

Common etiologies of rhabdomyolysis

A
  • Muscle injury
  • Muscle ischemia
  • Drugs or toxins
  • Exertional
  • Infection
  • Inflammation (autoimmune muscle damage)
  • Body temperature
  • Metabolism disorders and blood supply issues
76
Q

What can cause muscle injury leading to rhabdomyolysis

A
  • Crush trauma
  • Deep burns
  • Bite wounds
  • Necrotizing myopathy
77
Q

What can cause muscle ischemia leading to rhabdomyolysis

A
  • Shock
  • Localized compression
  • Immobilization
  • Compartment syndrome
78
Q

What drugs or toxins can cause rhabdomyolysis

A
  • ETOH
  • Statins
  • Fibrates
  • Antipsychotics
  • SSRIs
  • Benzos
  • Recreational drugs
  • Salicylates
  • Thrombolytics
  • Chemo agents
79
Q

What exertional factors can cause rhabdomyolysis

A
  • Intense physical exercise
  • Seizures
80
Q

What infections can cause rhabdomyolysis?

A
  • Coxsackie virus
  • Influenza A and B
  • Epstein Barr virus
81
Q

What can cause body temp change leading to rhabdo

A
  • Hyperthermia/heat illness
  • Hypothermia
82
Q

what are metabolism disorders and blood supply issues that can cause rhabdo

A
  • Thrombosis
  • Embolism
  • Clamping of artery in surgery
83
Q

Clinical presentation of rhabdomyolysis

A
  • Dark “tea colored” urine
  • Myalgias and weakness
  • Malaise
  • Low-grade fever
  • N/V, abdominal pain, and tachycardia in severe rhabdomyolysis
  • Swelling and tenderness of the involved muscle groups may occur, may not become apparent until after rehydration with IV fluids
  • Mental status changes if severe renal failure due to urea-induced encephalopathy
84
Q

Diagnostics for rhabdomyolysis

A
  • CK: most sensitive indicator
  • UA: reddish bronw color when urine myoglobin >100 mg/dL; + blood on dip, with negative RBC on microscopic suggests myoglobinuria
  • Urine myoglobin
  • CMP
  • Phosphorus: elevated
  • Uric acid: elevated
  • EKG: dysrhythmias related to hyperkalemia or hypocalcemia possible
  • CBC and coags to loos for DIC
  • Imaging: if underlying etiology requires
85
Q

How is CK associated with rhabdomyolysis

A
  • Direct reflection of amount of muscle injury
  • Levels typically 5x upper limit normal and rise 2-12 hours after onset of muscle injury, peaks within 24-72 hours
86
Q

What will be present on CMP in rhabdomyolysis?

A
  • Elevated K+
  • Hypocalcemia early in course, followed by hypercalcemia during recovery
  • BUN, Cr - elevated if AKI
  • AST/ALT - elevated
87
Q

Management of rhabdomyolysis

A
  • IV fluids: early and aggressive .9% NS @1-2 L/hr and titrate to UO goal for up to 72 hours MONITOR FOR FLUID OVERLOAD in heart/renal patients
  • I&O: insert foley to get accurate output measurements (goal of 200-300 mL/h)
  • Urine alkalization
  • Cardiac monitoring and serial EKGs
  • Electrolytes
  • Lab monitoring
88
Q

Goal of output in rhabdomyolysis

A
  • 200-300 mL/hr UO
89
Q

Indications for urine alkalinization

A
  • CK levels higher than 500 IU/L
  • Acidemia
  • Dehydration
  • Underlying renal disease
90
Q

Regimen for urine alkalinization

A
  • 150 mEq of sodium bicarbonate added to 1 L of 5% dextrose or water
  • Administered at 200 mL/hr with goal urine pH of >6.5
91
Q

How are electrolytes managed in rhabdomyolysis

A
  • Treatment of hyperkalemia with IV insulin (with IV glucose) and IV calcium (only if severe hyperkalemia in presence of hypocalcemia)
  • Hypocalcemia treatment if severe hyperkalemia
  • Phosphate and uric acid rarely need treatment
92
Q

Lab monitoring for rhabdomyolysis

A
  • CK q6 h - peak CK levels >6000 IU/L increase risk of AKI
  • K+ 1-2 hours after initiation of treatment
  • Glucose every hour if treating hyperkalemia with insulin/glucose
93
Q

When should nephrology be consulted about rhabdomyolysis

A
  • Oliguric renal failure
  • Persistent electrolyte abnormalities/acidosis
  • Signs of fluid overload
94
Q

When should ortho/surgery be consulted for rhabdomyolysis

A
  • Concern for compartment syndrome
95
Q

Disposition of rhabdomyolysis

A

Discharge criteria after rehydration:
* Normal renal function
* Normal electrolytes
* Alkaline urine
* An isolated cause of muscle injury
* No uncontrolled comorbidities

96
Q

Complications of rhabdomyolysis

A
  • Acute kidney injury: risk increases with dehydration, sepsis, and acidosis
  • Compartment syndrome: a potential complication of severe rhabdomyolysis that may develop after fluid resuscitation, with worsening edema of the limb and the muscle
  • Disseminated intravascular coagulation: occurs in severe rhabdomyolysis due to release of thromboplastin and other prothrombotic substances from damaged muscle
97
Q

What is fibromyalgia

A
  • Chronic
  • Widespread MSK pain with multiple tender points
  • No clear objective findings
  • One of most common rheumatologic syndromes affecting 3-10% of the general population
98
Q

What is the MC population impacted by fibromyalgia

A

Women aged 20-55

99
Q

Hypothesis of etiology of fibromyalgia

A
  • Presence of central sensitization to pain and deficits in endogenous pain inhibitory mechanism
  • Sleep disorders
  • Depression
  • Viral infections
100
Q

Clinical presentation of fibromyalgia

A
  • Chronic fatigue and generalized aching pain
  • Prominence of pain around neck, shoulders, low back, and hips
  • Most days for >3 months
  • Worsened by minor exertion
101
Q

What are associated symptoms/conditions with fibromyalgia

A
  • Depression
  • Anxiety
  • Sleep disorders
  • Cognitive dysfunction
  • Subjective numbness
  • Fatigue
  • Chronic headaches
  • IBS
102
Q

What is the PE in fibromyalgia

A

Normal, except for widespread soft tissue tenderness
Joints unaffected

103
Q

ACR New diagnostic criteria for fibromyalgia

A
  1. Widespread pain index (WPI) >7 and symptom severity (SS) > 5 OR WPI 3-6 and SS scale >9
  2. Symptoms have been present for at least three months
  3. There is no other disorder that would explain the patient’s symptoms
104
Q

Fibromyalgia is a diagnosis of ….

A

exclusion you must consider and rule out differential diagnoses

105
Q

General Management of fibromyalgia

A
  • Mutlidisciplinary approach is most effective
  • Reassurance the condition is diagnosable and treatable
  • Goals to improve function and quality of life rather than elimination of pain
  • Patient education essential: non-progressive course, treatment available but not curable, compliance and expectations regarding treatment key to success
106
Q

Non-pharmacologic treatment for fibromyalgia

A
  • Cognitive behavioral therapy: focus on sleep hygiene and mood disorders
  • Exercise: low aerobic activity with slow progression (aqua aerobics) to strength training
  • Weight loss if overweight
107
Q

Pharmacologic management for fibromyalgia

A
  • Muscle relaxant: cyclobenzaprine (flexeril)
  • Antidepressants: amitriptyline (elavil), duloxetine (cymbalta), milnacipran (savella)
  • Anticonvulsants: gabapentin (neurontin), pregabalin (lyrica)
  • Analgesic: tramadol (ultram)
  • Avoid opioids and corticosteroids
108
Q

How are most patients treated for fibromyalgia

A
  • Most patients initial cyclobenzaprine or amitriptyline at bedtime
  • Severe fatigue: start SNRI (cymbalta/savella)
  • Severe sleep disturbance: start with neurontin or lyrica
109
Q

What is neurogenic arthropathy?

A
  • Condition characterized by progressive destruction of bone and soft tissues at weight bearing joints
  • Leads to joint dislocations, pathologic fractures, and debilitating deformities
  • Hallmark deformity is midfoot collapse: “rocker-bottom” foot
110
Q

Pathophysiology of neurogenic arthropathy

A
  • Unknown but multifactorial
  • Neuro-traumatic
  • Neurovascular
111
Q

Etiology of neurogenic arthropathy

A
  • Condition that causes sensory or autonomic neuropathy
  • DM- most common
  • Cerebral palsy
  • Alcoholic neuropathy
  • Spinal cord injury
  • Syphilis
112
Q

Anatomy of neurogenic arthropathy

A
  • MC foot and ankle
  • MC joints: Tarsometatarsal joint
  • Cuneonavicular, talonavicular, and calcaneocuboid articulations
113
Q

Diagnostics for neurogenic arthropathy

A
  • Labs case based for underlying etiologies
  • X-ray: weight bearing if possible
  • MRI: if x-ray is negative or if osteomyelitis in ddx; sensitive for early disease showing bone marrow edema with or without microfracture and helps r/o osteomyelitis
114
Q

How does xray present with neurogenic arthropathy?

A
  • Normal or nonspecific in early disease
  • Soft tissue swelling, loss of joint space, osteopenia
  • As disease progresses: fractures
  • Subluxation and frank dislocations
115
Q

What can you see on progression of neurogenic arthropathy on xray?

A
  • Progressive decrease of calcaneal inclination
  • Equinus deformity at the ankle (inability to dorsiflex
  • Destruction of the tarsometatarsal joint with the typical rocker-bottom deformity
116
Q

What are characteristics of stage 0 neurogenic arthropathy?

A
  • Early or inflammatory
  • Localized swelling
  • Erythema
  • Warmth
  • Xray: little or no radiological abnormalities
116
Q

What are characteristics of stage 1 neurogenic arthropathy?

A
  • Development
  • Swelling
  • Redness
  • Warmth persisting
  • Xray: bony changes such as fracture, subluxation/dislocation, bony debris
117
Q

What are characteristics of stage 2 of neurogenic arthropathy?

A
  • Coalescence
  • Clinical signs of inflammation decrease
  • Xray: fracture healing, resorption of bony debris, and new bone formation
118
Q

What are characteristics of stage 3 of neurogenic arthropathy?

A
  • Remodeling
  • No signs of inflammation
  • Bony deformity, which may be stable or unstable, is present
  • X-ray: may show mature fracture callus and decreased sclerosis
119
Q

Management of stage 0-2 neurogenic arthropathy

A
  • Refer to a specialist experienced in treating condition: rheumatology, orthopedist, podiatrist
  • Avoid weight bearing –> use casting to offload the affected foot
  • Continue until signs of inflammation resolve and improvement in radiologic findings
  • Followed by the gradual progression to normal weight bearing with prescription footwear
120
Q

What is management of stage 3 neurogenic arthropathy?

and those who fail offloading therapy

A

discuss risk/benefit of surgery

121
Q

What is Raynaud’s phenomenon?

A

Syndrome of paroxysmal digital ischemia, most commonly caused by an exaggerated response of digital arterioles to cold or emotional stress

122
Q

Pathophysiology of Raynaud’s

A
  • Vasoconstriction leading to well-demarcated digital pallor or cyanosis followed by rapid vasodilation resulting in intense hyperemia and rubor
123
Q

Anatomy of Raynaud’s

A

MC affects fingers, but it can affect toes, nose and ears

124
Q

Primary classification of Raynaud’s

A
  • No vascular structural abnormalities
  • Exaggeration of normal vasoconstriction to cold exposure
  • MC onset in healthy females between 15 and 30 years of age
    • FMHx in 30% of patients
125
Q

Secondary classification of Raynaud’s

A
  • Underlying condition leads to RP
  • MC onset in male over age 40
  • MC associated with rheumatologic conditions: systemic sclerosis, SLE, sjogren, or dermatomyositis
  • Other risk factors/precipitating events: frostbite, chronic use of certain tools (ie jackhammer)
  • Symptoms more severe with increased risk of digital ulceration or gangrene
125
Q

Presentation of Raynaud’s phenomenon

A
  • Sudden onset of cold digits with a demarcation of skin pallor (white attack) or cyanosis (blue attack)
  • White attacks more likely to lead to digital ischemia
  • During rewarming, there is vascular reperfusion, resulting in erythema secondary to rebound blood flow
  • Associated symptoms: aching or throbbing pain, paresthesia, numbness, stiffness, mild swelling may occur after rewarming
  • Sclerodactyly
  • Calcinosis
  • Digital ulcers
126
Q

Location of Raynaud’s phenomenon

A
  • Early in course single finger
  • With time multiple fingers of both hands
  • MC digits: index, middle, and ring fingers
127
Q

What tool can help with diagnosis of raynaud’s phenomenon

A
  • Opthalmoscope to magnify nailfold capillaries: abnormally large loops, alternating areas without any capillaries
  • Enlarged or distorted capillary loops and/or dropout or loss of loops suggest an underlying autoimmune rheumatic disease
128
Q

Management of primary Raynaud’s phenomenon

A
  • Patient education
  • Follow up regularly to ensure signs and/or symptoms of secondary causes of raynaud’s phenomenon do not emerge
  • RP is occasionally 1st manifestation of these disorders
129
Q

Management of secondary Raynaud’s phenomenon

A
  • Order labs to look for underlying causes –> individually based upon H&P
  • Treat underlying disease
130
Q

What patient education should be provided to a patient with Raynaud’s phenomenon?

A
  • Wear mittens and stockings when outside in cold weather
  • Avoid vasoconstricting medications: decongestants, diet pills, sumatriptan, opiates
  • Smoking cessation
  • Refer to vascular surgery if resistant to pharmacologic therapy
131
Q

Pharmacologic therapy for Raynaud’s phenomenon

A
  • If failure to control symptoms with non-pharm therapies or if evidence of digital ulcers
  • CCB’s - first line: amlodipine 5-20 mg/d
  • Topical vasodilators, PDE5 inhibitors
132
Q

What is Marfan’s syndrome?

A

Genetic disorder of the connective tissue characterized by skeletal, ocular, and cardiovascular abnormalities; affects 1 in 5000 patients

133
Q

Presentation of Marfan syndrome

A
  • Typically tall, with long arms, legs, and digits
  • Scoliosis
  • Pectus excavatum/carinatum
  • Ectopia lentis is present in about 1/2 of patients
  • Severe myopia
  • Retinal detachment can occur
  • Mitral valve prolapse in 85% of patients
  • Aortic root dilation common and leads to aortic regurgitation or dissection with rupture
134
Q

Diagnostics for marfan syndrome

A
  • Echocardiogram/abdominal US to assess aorta
  • Slit lamp exam to check lens displacement
  • Genetic testing: mutations in the fibrillin gene on chromosome 15
135
Q

What criteria is used to diagnose Marfan syndrome?

A

Ghent scoring system

136
Q

Management of Marfan Syndrome

A
  • Annual opthalmologic evaluation: monitor and correct visual acuity and prevent amblyopia
  • Annual orthopedic consultation: monitor development of scoliosis at early age to brace and delay progression
  • Echo annually to monitor aorta diameter and mitral valve function, follow with cardiology annually and surgical intervention may be necessary
  • Long term beta blockers slows rate of aortic dilation: atenolol or metoprolol
  • Restriction from vigorous physical exertion to prevent aortic dissection
137
Q

Prognosis of Marfan syndrome

A
  • Results in death in 4th or 5th decade from aortic dissection or heart failure secondary to aortic regurgitation in untreated marfans
  • Life expectancy increased with early diagnosis, lifestyle modifications, beta-adrenergic blockade, and prophylactic aortic surgery

MSK (11 decks)

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