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Year 2 > MSK: Part 7 > Flashcards

MSK: Part 7 Flashcards

1
Q

How does meningococcal arthritis occur

A
  1. Deposition of circulating immune complexes containing meningococcal antigens
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2
Q

How is meningococcal arthritis treated

A

PENICILLIN

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3
Q

What causes tuberculous arthritis

A

MYCOBACTERIUM TUBERCULOSIS

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4
Q

What joints are commonly effected in tuberculous arthritis

A

Hip
Knee
Intervertebral discs

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5
Q

Pathophysiology of tuberculous arthritis

A

caveating granulomas

Rapid destruction of cartilage and adjacent bone

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6
Q

Clinical presentation of tuberculous arthritis

A

Fever
Night Sweats
Weight Loss

Pain, swelling and dysfunction

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7
Q

Diagnosis of tuberculous arthritis

A
  1. Culture synovial fluid
  2. Biopsy synovial fluid or intervertebral disc - CT guided
  3. X-ray may be normal but shows joint-space reduction and bone destruction
    4
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8
Q

Treatment for tuberculous arthritis

A

9 months:

Rest joint and spine immobilised in cute phase

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9
Q

What is osteomyelitis

A

Bone marrow inflammation localised to one bone

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10
Q

What causes osteomyelitis

A

Haematogenous spread or due to local infection

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11
Q

What age group is effected by osteomyelitis

A

Children

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12
Q

How do adults get osteomyelitis

A

Secondary infection or direct trauma

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13
Q

Main causes of osteomyelitis

A
  1. Staph Aureus
  2. Coagulase negative staphylococci
  3. Haemophilus influenza
  4. Salmonella (SSA)
  5. Pseudomonas aeriguinosa and seratia marcesans in IVDU
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14
Q

Risk factors for osteomyelitis

A
  1. Diabetes mellitus
  2. Peripheral vascular disease
  3. Malnutrition
  4. Inflammatory arthritis
  5. Debilitating disease
  6. Decreased immunity
  7. Sickle cell disease
  8. Immunosuprresive drugs
  9. Trauma
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15
Q

Two ways bacteria can get into th bone

A
  1. Direct inoculation of infection into the bone via trauma
  2. Contigous spread of infection into the bone (not as easy):

Without breaking skin
Infection of adjacent soft tissue spreading into bone

Haematogenous seeding (hard to do)

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16
Q

What age group usually has osteomyelitis caused by spread of infection into th bone

A 
Elderly:
Diabetes mellitus
Chronic ulcers
Vascular disease
Joint replacement 
Prostheses
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17
Q

What is haematogenous seeding

A

Infection from skin spreading to the blood then to the bone (Staphylococcus aureus from cannula on skin to blood then into bone)

EXAMPLE

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18
Q

What bones are usually effected in children in haematogenous seeding

A

Long bones - metaphysics (wide portion of a long bone between the epiphysis and the narrow diaphysis - contains growth plate) of the long bone

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19
Q

Why is the metaphysis most commonly effected in haematogenous seeding

A
  1. Here blood flow is slower, endothelial basement membrane is absent and the capillaries lack or have inactive phagocytic lining cells - all these factors predispose to bacteria migrating from blood into bone and the growth of bacteria in the bone
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20
Q

Where is haemotgenous seeding in adults

A

Vertebra

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21
Q

Why is the vertebra target for haematogenous seeding

A

With age, vertebra becomes more vascular thereby making bacterial seeding of the vertebral endplate more likely

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22
Q

What condition can cause risk for haematogenous seeding

A
  1. IVDU (in younger - clavicle and pelvis)
  2. Dialysis
  3. Sickle cell disease
  4. Urethral catheterisation and UTI
  5. Endocarditis
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23
Q

What bone does sickle cell disease cause bacteraemia in

A

Vascular necrosis of the hip

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24
Q

Acute changes to cells in osteomyelitis

A
  1. Inflammatory cells
  2. Oedema
  3. Vascular congestion
  4. Small vessel thrombosis
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25
Q

Chronic changes to cells in osteomyelitis

A
  1. Necrotic bone ‘sequestra’
  2. New bone formation - involucrum
  3. Neutrophil exudates
  4. Lymphocytes and histiocytes (tissue macrophages)
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26
Q

Pathophysiology of osteomyelitis

A
  1. Inflammatory exudates in the marrow leads to increased intramedullary pressure, with extension of exudate into bone cortex
  2. Causes rupture through periosteum and interruption of periosteal blood supply resulting in necrosis
  3. This leaves sequestra
  4. New bone called involucrum forms over it
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27
Q

What is sequestra

A

Pieces of separated dead bone

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28
Q

Clinical Presentation of osteomyelitis

A
  1. Dull pain at site that is aggravated by movement
  2. Fever, sweats, riggers and malaise
  3. ACUTE: Tenderness, warmth, erythema and swelling
  4. CHRONIC: Tenderness, warmth, erythema and swelling
    Draining sinus tract which is associated with deep/large ulcers that fail to heal despite treatment
  5. SEPTIC ARTHRITIS
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29
Q

Symptoms if osteomyelitis occurs in the hip, vertebrae or pelvis

A

Pain and that’s it

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30
Q

Why would osteomyelitis result in septic arthritis

A
  1. When infection breaks through cortex resulting in discharge of pus into the joint - knee, hip or shoulder
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31
Q

Where is septic arthritis caused by osteomyelitis common

A

Infants - patent transphyseal blood vessels and immature growth plates

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32
Q

Differential diagnosis of osteomyelitis

A
  1. CHARCOT JOINT - damage due to sensory nerves affected by diabetes
  2. Soft tissue infection (cellulitis and erysipelas)
  3. Avascular necrosis of the bone causes: steroids, radiation or bisphosphonate use)
  4. Gout
  5. Fracture
  6. Malignancy
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33
Q

Diagnostics of osteomyelitis

A
  1. Imagine (X-rays, bone scans and MRI)
  2. FBC
  3. Bone biopsy and culture to determine aetiology
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34
Q

What would an x-ray show in osteomyelitis

A
  1. Osteopenia
  2. Cortical erosions
  3. Sclerosis
  4. Sequestra
  5. Soft tissue swelling
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35
Q

When is an MRI for osteomyelitis done

A

Marrow oedema from 3-5 days
Soft tissue inflammation

AFTER X-ray (takes time for changes to be seen)

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36
Q

FBC results in osteomyelitis

A
  1. ESR and CRP raised
  2. Raised WCC in acute
  3. Chronic osteomyelitis - normal WCC
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37
Q

How is osteomyelitis treated

A
  1. Immobilisation
  2. IV TECLOPANIN
  3. IV FLUCOXACILLIN
  4. ORAL FUSIDIC ACID
  5. ESR and CRP monitoring
  6. Removal of dead bone (sequestrium)
38
Q

How is tuberculous osteomyelitis caused

A

Haematogenous spread from a reactivated primary focus in lungs or GI tract

39
Q

Clinical presentation of tuberculous osteomyelitis

A
  1. Local Pain

2. Swelling if pus collected

40
Q

Diagnostics for tuberculous osteomyelitis

A
  1. BIOPSY - caveating granuloma
41
Q

Treatment for tuberculous osteomyelitis

A
  1. 12 months with same treatment as for pulmonary tuberculosis
42
Q

Where does prosthetic joint infection happen

A

Hips and Knees

43
Q

Main causes of prosthetic joint infection

A

Staph A
Coagulase negative staphylococci (most frequent after hip replacement)
Gram-POSITIVES

44
Q

Risk factors for Prosthetic joint infection

A
  1. Poor infection control
  2. Old age
  3. Diabetes
  4. Obesity
45
Q

How do you prevent infections in prosthetic joints

A
  1. Plastic screen that walls off the anaesthetist from joint
  2. Lamina flow theatres with filtered air blowing out of the theatre to make it difficult for organisms to enter
  3. Antibiotics placed into bone cement and systemic antibiotics pre-op help minimise infection risk
46
Q

Clinical presentation of prosthetic joints

A
  1. Not acutely infected
  2. Systemically well
  3. Tender, hot, swollen joint
47
Q

Diagnostics for prosthetic joints

A
  1. Tissue sample from surgery
  2. ESR and CRP raised
  3. Alpha defensive
  4. Joint aspiration - GOLD STANDARD
48
Q

Why is joint aspiration the gold standard for prosthetic joints

A
  1. Identifies organisms and antibiotic sensitivities

2. MUST BE DONE OFF ANTIBIOTICS FOR 2 WEEKS MINIMUM

49
Q

Treatment for prosthetic joints

A
  1. Antibiotics suppression
  2. Debridement and retention of prosthesis
  3. Excision arthroplasty
  4. One-stage arthroplasty exchange
  5. Two-stage arthroplasty exchange
    6/ A,mutation in severe infection
50
Q

What are the aims of treatment in prosthetic joint infections

A
  1. Eradicate sepsis
  2. Relieve pain
  3. Restore function
51
Q

When is excision arthroplasty done

A

High risk frail and co-morbidities who have infection that is uncontrolled with antibiotic suppression

  1. People with low functional demand
  2. Effectie in removing infection but not good at restoring function
52
Q

What is one-stage arthroplasty exchange

A
  1. Radical debridement
  2. Implantation of new prosthesis with antibiotic cement
  3. Systemic and local antibiotics
  4. Avoid bone graft
  5. 85% success rate
53
Q

What is two-stage arthroplasty exchange

A
  1. radical debridement
  2. Local antibiotic spacer +/- systemic antibiotics
  3. Interval stage (suture up and wait for infection to clear)
  4. Implantation of new prosthesis with antibiotic cement
  5. Routine antibiotic prophylaxis
  6. 90-95% success
54
Q

Define major trauma

A
  1. Serious and often multiple injuries where there is a strong possibility of death or disability with an injury severity score greater than 15
55
Q

What is an injury severity score

A
  1. Each injury is scored depending on the abbreviated injury scale
  2. Assigned to one of six body regions:
    Head + Neck
    Face
    Chest
    Abdo
    Extremity - pelvic skeleton
    external
56
Q

What is the Abbreviated injury scale

A
  1. Minor - Superficial Laceration
  2. Moderate - Fractured sternum
  3. Serious - Open fracture humerus
  4. Severe - Perforated trachea
  5. Critical - Ruptured Liver
  6. Unsurvivable - Total aortic transection
57
Q

How is an ISS score made

A

Only the highest score in each region is counted

The 3 highest scores are counted and then squared and then x3 to generate ISS

Score of 6 in any region gets automatic ISS of 75

58
Q

What is Juvenile Idiopathic Arthritis

A

Joint swelling/Stiffness/limitation in those older than 6 weeks but under 16 with not other causes
7 subtypes according to presentation

59
Q

What doctor would a child age 15 see

A

Paediatrician

Normal doctor over 16

60
Q

What usually causes idiopathic arthritis

A

Autoimmune

Gene combinations

  1. infection
  2. Reactive
  3. Trauma
  4. Malignancy
  5. Connective tissue disease
61
Q

What pathologies can be seen in Juvenile Idiopathic Arthritis

A
  1. Synovitis
  2. Persistent oligoarthritis
  3. Extended oligoarthritis
  4. Rheumatoid factor negative polyarthritis
  5. Rheumatoid factor positive polyarthritis
  6. Enthesitis
  7. Stills disease
62
Q

What are children with JIA at high risk of

A

UVEITIS - membrane lining the eyes is similar to that of joint and suffer from CHRONIC ANTERIOR UVEITIS

They can go blind

63
Q

How do we prevent uveitis in juvenile idiopathic arthritis

A

OPTHALMIC SCREENING EVERY 3 Months

64
Q

In what individuals is persistent oligoarthritis found in

A

Less than 6

65
Q

What joint is effected in persistent oligoarthritis

66
Q

Diagnosis for JIA with persistent oligoarthritis

A

ANA negative

HIGH RISK UVEITIS

67
Q

Treatment for persistent oligoarthritis in JIA

A

Grow out of it so leave

68
Q

What gender is extended oligoarthritis usually effecting

69
Q

Peak age of extended oligoarthritis

70
Q

What has a worse prognosis extended or persistent

71
Q

What risk is associated with extended oligoarthritis

72
Q

What defines rheumatoid factor negative polyarthritis in JIA

A

Acute or insidious onset in more than 5 joints

73
Q

Clinical features of rheumatoid factor negative polyarthritis

A

SYMMETRICAL
malaise, fever and anaemia
UVEITIS

74
Q

When does rheumatoid factor positive polyarthritis manifest

A

Late adolescent in girls

75
Q

What condition is rheumatoid factor positive polyarthritis similar to

76
Q

FBC in rheumatoid factor positive polyarthritis

A

CCRP antibody is negative

77
Q

Risk in RFPP

A

UVEITIS

related to smoking

78
Q

When does enthsitsis related JIA occur

A

HLA-B27 positive - spondyloarthritis in young people

79
Q

What age does enthesitis related JIA occur

A

MALES OVER 6

HIGH RISK UVEITIS

IBD associated

80
Q

Symptoms of enthesitis related JIA

A

IBD

Inflammatory back pain or sacroiliac pain

81
Q

When does Stills disease occur

82
Q

What is stills disease

A

Systemic illness with daily fever - fever spikes daily at same time

Evanscent rash and artritis

Anaemic, raised platelets and high ferritin

Lymphadenopathy , hepatosplenomegaly and serositis

83
Q

Non-medical Treatment for JIA

A
  1. Information and education
  2. Support and liaison with school
  3. Physiotherapy
  4. Occupational therapy
  5. Psychology
84
Q

Medical treatment for JIA

A
  1. Steroid joint injections - ENTONOX (laughing gas) for general anaesthetic
  2. IBUPROFEN
  3. METHOTREXATE
  4. Systemic steroids
  5. IV INFLIXIMAB
85
Q

Where is osteomyelitis seen in children

A

Arms + Feet

86
Q

Where is osteomyelitis seen in adults

A

Feet
Spine
Hips

87
Q

How does TB spread from ling to bone

A

HAEMATOGENOUS SPREAD

88
Q

Pathophysiology of osteomyelitis

A

Leukocytes invade bone to try engulf pathogens

However produces pus which spreads into blood vessels and blocks blood = sequestra

Bone trys producing now bone to replace necrosed bone = involucrum

89
Q

Complication of osetomyelitis in children

A

Subperiosteal abscesses

90
Q

What two types of osteomyelitis is there

A

Sclerotic (increased bone density)

Suppurative (pus filled)

91
Q

What is involucrum

A

Layer of new bone outside existing bone

92
Q

Bone biopsy in osteomyelitis

A
  1. 16sRNA PCR

2. Inflammation and osteonecrosis

Year 2 (155 decks)

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