Musculoskeletal Disorders Flashcards

1
Q

Define Slipped Upper Femoral Epiphysis

A

Occurs when weakness in the proximal femoral growth plate allows displacement of the
epiphysis of the femoral head postero-inferiorly

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2
Q

What is the pathophysiology of SUFE

A

• Rare hip condition mainly seen in OBESE BOYS
• Pathophysiology
o Normally femur consists of 4 parts
▪ Diaphysis (shaft of the bone)
▪ Metaphysis
▪ Neck
▪ Physis/growth plate: contains cell which divide and allow bone to grow in length→growth plate eventually ossifies and fuses with the epiphysis (~age 16 in females and age 19 in males)

o During growth spurt, the growth plate is relatively weak and vulnerable to shearing forces

o Before the growth plate ossifies, it is supported by the perichondrial ring (dense connective tissue that extends from the metaphysis to the epiphysis). The perichondrial ring helps resist shearing forces so that the femoral head and femoral neck don’t slip away from one another

o In slipped capital femoral epiphysis, the perichondrial ring becomes too weak to resist the shearing forces between the femoral head and neck causing the two gradually slip away from each other

o It is not actually the epiphysis that slips away→it is the neck that displaces anterolaterally and superiorly

o If the displacement is severe, it can tear the epiphyseal blood vessels interrupting the blood supply to the femoral head. If this happens, it can lead to avascular necrosis of the femoral head
• Requires prompt treatment to prevent avascular necrosis

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3
Q

What are the RFs of SUFE?

A

• Most common at ages 10-15 years during adolescent growth spurt, particularly in obese boys
• Risk factors
o OBESITY: the extra weight increases pressure on the epiphysis-physis junction
o Rapid growth during adolescence
o There is an association with metabolic endocrine abnormalities e.g. hypothyroidism
and hypogonadism o Family history

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4
Q

What are the clinical features of SUFE?

A
  • May present acutely following trauma or more commonly with chronic, persistent symptoms
  • Acute (after minor trauma) or insidious onset of pain and limp
  • Bilateral in 20%
  • Hip, groin, medial thigh or knee pain
  • Examination shows restricted abduction and internal rotation of the hip
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5
Q

What investigations would you do for a suspect SUFE

A

X-ray including frog lateral view

o Bilateral AP X-ray will show Klein’s line, which is drawn along the superior aspect of the femoral neck, not intersecting the femoral head (normally intersects some part of the femoral head) - Trethowan’s sign

o Frog-leg lateral X-ray will show Bloomberg’s sign (physis will be blurred or widened), widened joint space and displaced femoral head

MRI if high suspicion - can detect early SUFE or features consistent with a risk of slipping in the contralateral hip.

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6
Q

What is the management of SUFE?

A

Don’t let the patient walk, analgesia- Period of rest with limited weight bearing

Surgical repair - In situ screw fixation across the growth plate - immediate orthopaedic referral

Physiotherapy post surgery to regain normal function

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7
Q

How does arthritis present?

A

Acute arthritis presents with pain, swelling, heat, redness and restricted movement in a joint

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8
Q

What are the type of arthritis?

A

Monoarthritis and polyarthritis

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9
Q

What are the causes of monoarthritis?

A

o Septicarthritis

o Osteomyelitis

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10
Q

What are the causes of poly arthritis?

A
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11
Q

What is the most common arthritis in childhood?

A

Reactive arthritis.

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12
Q

What is reactive arthritis?

A

An inflammatory arthritis that occurs following exposure to certain gastrointestinal and genitourinary infections

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13
Q

What are the preceding extra-articular infections in reactive arthritis?

A

o Common preceding infections in childhood are enteric bacteria including Salmonella,

Shigella, Campylobacteria, Yersinia

o Other causes:

▪ Viral infections

▪ STIs in adolescents: chlamydia, gonococcus

▪ Mycoplasma

▪ Borrelia burgdorferi (Lyme disease)

▪ Rheumatic fever and post-streptococcal reactive arthritis, particularly in developing countries

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14
Q

What are the clinical features of reactive arthritis?

A
  • History of gastrointestinal or genitourinary infection 1-4 weeks before onset of arthritis
  • Transient joint swelling of ankles or knees usually
  • Low grade fever

Characterised by transient joint swelling (usually < 6 weeks) often of the ankles or knees

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15
Q

What would investigations for reactive arthritis show?

A

ESR/CRP: mildly elevated

Urogenital/stool culture

X-ray: normal

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16
Q

What is the management for reactive arthritis?

A

No treatment is required as it is self-resolving

Symptomatic relief:

o NSAIDs for pain-relief

o Steroids (severe)
o DMARDs (on-going)
17
Q

Define septic arthritis.

A

Infection of one or more joints due to pathogenic inoculation of microbes → serious as can lead to bone destruction

18
Q

What causes septic arthritis?

A

o Usually due to haematogenous seeding from a distant infection

o Less commonly, can occur due local extension of local sepsis, iatrogenic implantation or post-trauma

o In young children, it may result from adjacent osteomyelitis into joints where the capsule inserts below the epiphyseal growth plate

19
Q

What age group are typically affected by septic arthritis?

A

< 4 yrs old

20
Q

What are the causative organisms of septic arthritis?

A

• Causative organism

o STAPHYLOCOCCUSAUREUS= most common post neonatal period
o < 3 months: STAPH AUREUS, Group B Strep
o 3 months – 5 years: Kingella kingae, STAPH AUREUS, beta-haemolytic streptococci, Strep pneumoniae, meningococcus (rarely Hib)
o > 5 years: Staph aureus, beta-haemolytic Streptococci
o Sickle cell disease: S aureus is still most common but salmonella also associated with SCD
o Neisseria gonorrhoea: adolescents

21
Q

What joint is most commonly affected in septic arthritis?

A

Hip (75%), knees and ankles can also be affected

22
Q

What are the risk factors of septic arthritis?

A

o Underlying illness e.g. immunodeficiency, sickle cell disease

23
Q

What are the clinical features of septic arthritis?

A
  • PAINFUL, HOT, SWOLLEN, RESTRICTED JOINT
  • Acutely unwell, febrile child
  • Infants may hold the limb still (pseudoparesis, pseudoparalysis)
  • Infants will cry when the affected limb is moved
  • Joint effusion may be visible in peripheral joints
  • Co-existent osteomyelitis (15%) - marked tenderness over bone
  • Pain may be referred to the knee
  • May present with limp initially
  • Often diagnosed late due to poor localisation of symptoms and normal plain X-ray findings
24
Q

What are the investigations for septic arthritis?

A

WCC

Raised acute-phase proteins: CRP, ESR

Blood cultures

Ultrasound of deep joints (hip) (reveal an effusion)

X-rays to exclude trauma

o Changes not usually seen until 2-3 weeks after

o May show widening of joint space, soft tissue swelling and ill-defined articular margins

Aspiration under ultrasound guidance is the definitive investigation

o This should be performed IMMEDIATELY

o Synovial fluid Gram stain and culture
o Synovial fluid WCC

MRI
o Done if high index of suspicion

25
Q

What is the criteria used for assessing septic arthritis?

A
26
Q

What is the management of septic arthritis?

A

Early treatment of septic arthritis is essential to prevent destruction of the articular cartilage and bone.

  • Prolonged course of antibiotics (initially IV for 2 weeks, followed by 4 weeks of oral antibiotics)
    • o Suspected Gram-positive
      • Vancomycin
      • 2nd line = clindamycin or cephalosporin
    • o Suspected Gram-negative
      • 3rd generation cephalosporin (e.g. ceftriaxone)
      • 2nd line = IV ciprofloxacin
  • Joint aspiration - affected joints should be aspirated to dryness as often as required (through closed needle aspiration or arthroscopically)
  • Washing out of the joint or surgical drainage may be required
  • Joint is initially immobilised in a functional position but must subsequently be mobilised to prevent permanent deformity
27
Q

What is the most common chronic inflammatory joint disease in children and adolescents in the UK?

A

Juvenile idiopathic arthritis.

28
Q

Define Juvenile Idiopathic

A

Persistent joint swelling (of > 6 weeks duration) presenting before 16 years of age in the absence of infection or any other defined cause

29
Q

What is the prevalence of JIA?

A

1 in 1000

30
Q

What are the subtypes of JIA?

A

o Oligoarthritis (persistent)

o Oligoarthritis (extended)

o Polyarthritis (RF negative)

o Polyarthritis (RF positive)

o Systemic arthritis

▪ Also known as Still’s disease

▪ Features: pyrexia, salmon-pink rash, lymphadenopathy, arthritis, uveitis, anorexia and weight loss (PASWUL)

o Psoriatic arthritis

o Enthesitis-related arthritis

o Undifferentiated arthritis

31
Q

How do we classify JIA?

A
o Polyarthritis = \> 4 joints
o Oligoarthritis (pauciarticular) = \< 4 joints
o Systemic = with fever and rash
o Other subtypes: psoriatic arthritis, enthesitis
o Subtyping can be further classified by the presence of rheumatoid factor and HLA- B27 tissue type
32
Q

What are the clinical features of JIA?

A

Gelling (stiffness after rest)

Morning stiffness

Joint pain

Young children: may present with intermittent limp or deterioration in behaviour or mood or avoidance of previously enjoyed activities

Joint swelling

o May be minimal at first
o Subsequently swelling due to fluid in joint, inflammation, chronic arthritis, proliferating (thickening) of synovium and swelling of periarticular soft tissues
o Pauciarticular: medium sized joints affected e.g. knees, ankles, elbows → may have limp

33
Q

What are the investigations for JIA?

A

• Baseline investigations may be initially normal

o FBC
o Inflammatory markers o Rheumatoid factor
o X-rays

o ANA may be present

In any child with widespread joint pain, fatigue or multisystem involvement, the possibility of a connective tissue disorder should be considered e.g. JIA or SLE

If systemic features are present, consider sepsis or malignancy

34
Q

What is the management of JIA? What is the prognosis?

A
  • Joint injections – effective, first-line treatment for oligoarticular JIA; in polyarticular disease multiple joint injections are used as a bridging agent when starting methotrexate. Often requires sedation or inhaled anaesthesia (Entonox). Depending on the joint, guidance with ultrasound or X-rays may be needed.
  • Cytokine modulators (‘ biologics ’) and other immunotherapies – many agents (e.g. anti-TNF alpha, IL-1, CTLA-4, or IL-6) are now available and useful in severe disease refractory to methotrexate. They are expensive and given under strict national guidance with registries for long-term surveillance. T-cell depletion coupled with autologous haematopoietic stem cell rescue (bone marrow transplant) is an option for refractory disease. Selecting the most suitable medication remains problematic.
35
Q

What are the complications of JIA?

A

o Bone expansion (leading to leg lengthening or valgus deformity, or discrepancy in digit length)

o Chronic anterior uveitis

▪ If not detected and treated, it could lead to severe visual impairment

▪ Should do regular ophthalmological screening using slit lamp (especially if oligoarticular disease or ANA positive)

o Flexion

▪ Occurs when the joint is held in the most comfortable position for a long time

▪ Can lead to joint destruction contractures of the joints

o Growth
▪ May be generalised from anorexia, chronic disease and systemic failure corticosteroid therapy

▪ Localised overgrowth can occur due to prolonged active knee synovitis

o Constitutional problems

o Macro­phage activation syndrome (MAS)

  • The most serious complication of systemic JIA is macro­phage activation syndrome (MAS), which occurs in 4%–13%.
  • Presentation is acute, with continuous fever, reduction in erythrocytes, leukocytes and platelets, abnormal clotting and multiple organ failure.
  • Without early recognition and prompt treatment, it is life-threatening.

o Osteoporosis

o Amyloidosis

36
Q
A

SUFE