Paediatric Musculoskeletal Disorders Flashcards

1
Q

Acute Arthritis

A

presents with the cardinal signs of inflammation; In Monoarthritis, typically systemically unwell with fever (Septic Arthritis, Osteomyelitis; Urgent management required)

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2
Q

Most common arthritis

A

Reactive Arthritis is the most common arthritis; Transient joint swelling often in Ankles/Knees;
o Low grade fever; Normal or mildly-elevated CRP, Normal XR
o NSAIDs, complete recovery anticipated

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3
Q

Causes of reactive arthritis

A

Often caused by Enteric bacteria (Salmonella, Shigella, Campylobacter, Yersinia); Viral Infections, STIs in adolescents (Chlamydia, Gonorrhoea), Mycoplasma and Lyme disease are other causes

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4
Q

Other causes of polyarthritis

A

Other causes of polyarthritis include Inflammatory Bowel Disease-related, Vasculitis-related (e.g. HSP, Kawasaki), Haematological and Malignant disease, Connective Tissue Disease

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5
Q

Septic Arthritis

A

Serious infection of joint space leading to Bone Destruction; Most commonly <2yrs; Mostly Haematogenous spread but can also be due to break in skin or infected lesions
• Typically, Mono or Oligoarthritis; Most common, beyond Neonatal period is S aureus; HiB used to be of concern but less so with immunisation
o Need to consider immunodeficiency or predisposing illness, such as Sickle Cell

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6
Q

Presentation of Septic Arthritis

A

Presents with Erythematous, Warm, acutely tender joint with reduced ROM in acutely unwell and febrile child; Infants often hold limb still (Pseudoparesis) and cry if moved
o Joint effusion; Bone tenderness if Osteomyelitis (up to 15% cases of Osteomyelitis have Septic Arthritis as well

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7
Q

Septic Hip

A

Septic Hip might be hard to identify due to subcutaneous fat protecting joint; Signs include Pseudoparesis, Limping gait or Knee referred pain

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8
Q

Septic Arthritis: Investigations

A

FBC, CRP, Blood Cultures
• US of deep joints to identify Effusion, XR to exclude trauma and other bone lesions
o XR normal in Septic Arthritis, other than Joint Space widening and Soft Tissue swelling
• US-Guided Aspiration with MC+S, Ideally, before antibiotics started;

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9
Q

Management of Septic Arthritis

A

Prolonged course IV Abx
o Initially joint immobilised while IV Abx; mobilisation after improvement
• Wash out or surgical drainage might be required if resolution does not occur rapidly, or for deep-seated infections

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10
Q

Juvenile Idiopathic Arthritis

A

Most common Chronic Inflammatory Joint disease; Persistent swelling >6/52 before 16yrs, in absence of infection of other cause; 1 in 1000
o 95% have disease clinically and immunogenetically different from RA

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11
Q

Juvenile Idiopathic Arthritis: Classification

A

Clinically classified, according to Number of joints affected, Systemic symptoms, or other Extra-articular features; Also, Rheumatoid Factor and HLA-B27 classified

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12
Q

Juvenile Idiopathic Arthritis: Presentation

A

Gelling (Stiffness after rest), Morning Joint Stiffness, Pain; May present as Intermittent Limp, Deterioration in Behaviour and Activity Avoidance
Initially only minimal evidence of joint swelling; Subsequently followed by Effusion, Inflammation, Chronic Arthritis, Synovial Proliferation and Periarticular Swelling

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13
Q

Complications of JIA

A
  • Uncontrolled disease can lead to Overgrowth Bone Expansion, resulting in Limb and Hand deformities; Flexion contractures can occur in longer term
  • Chronic Anterior Uveitis – Common but usually asymptomatic; If untreated, can lead to Cataract and Glaucoma; Requires regular Ophthalmic screening
  • Growth Failure – Anorexia, Chronic Disease, Systemic Corticosteroid therapy; May also be due to localised overgrowth due to inflammation and undergrowth due to premature fusion
  • Constitutional Problems – Anaemia of Chronic Disease and Delayed Puberty
  • Osteoporosis and Amyloidosis (rarely, high mortality from renal failure
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14
Q

JIA Prognosis

A

Good disease control and QOL if management concordance; Significant morbidity from previous inflammation, joint damage, visual impairment and fractures due to Steroid use; 1/3 will need treatment in adult years to maintain remission

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15
Q

Management of JIA: MDT

A

Deformity and Disability much less common with Early Diagnosis and new treatments; Aims to induce remission as soon as possible
o All suspected should be managed by Specialist Paediatric Rheum MDT;
o Education and Support for family; PT to maintain joint function, Ophthalmology etc

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16
Q

Management of JIA: Medication

A

NSAIDs and Analgesia – Non-disease modifying, but effective symptom relief
• Joint Injections (±US-guided) – Effective, First-line for Oligoarticular JIA; Used for bridging for Polyarticular JIA before starting Immunosuppression; Often requires sedation or Entonox
• Methotrexate – Early use reduces joint damage; 70% effective in Polyarthritis, requires regular blood monitoring (LFTs, BM Suppression); Nausea common
• Systemic Corticosteroids – Avoided if possible due to Growth Suppression and Osteoporosis risk; Pulsed IV Methylprednisolone for Severe Polyarthritis

17
Q

Management of JIA: What to use if refractory to methotrexate

A

Biologics – Useful for Severe Disease refractory to Methotrexate

18
Q

Management of JIA: Refractory Disease

A

T-cell depletion, followed by Autologous Haemopoietic Stem Cell Rescue if Refractory disease

19
Q

Rickets

A

Failure of Growing Bone Mineralisation; C/f Failure for Mature Bone = Osteomalacia

20
Q

Risk factors for Rickets

A

o Higher risk in children breastfed into late infancy, as well as Preterm infants, due to Phosphate deficiency, or low Calcium and Phosphate stores
o Malabsorption disorders – CF, Coeliac, Pancreatic Insufficiency; Fanconi Syndrome (Loss of Renal Phosphate)
o Drugs – Phenytoin, Phenobarbital interfere with Vitamin D Metabolism; Can also be deranged due to Hepatic and Renal Disease, and few Genetic disorders

21
Q

Signs of Rickets

A

Earliest sign is Craniotabes over Occiput or Parietal bones; Palpable Costochondral junctions (Rachitic Rosary), Wrists and Ankles may be widened; Harrison’s Sulcus of the Ribs

22
Q

Diagnosis of Rickets

A

Diagnosis based on Dietary History, Low Ca, Low Phos, High Alk Phos, Low 25-OH Vit D and High PTH; XR Wrist shows Cupping and Frays of Metaphysis, and Widened Epiphyseal plate

23
Q

Management of Rickets

A
Diet advice (Oily fish and Egg Yolk; Supplemented Milk, Cereals, Fruit Juice), Managing Predisposing factors, Daily Vitamin D3 (Cholecalciferol) ± Single high dose prior
o Healing occurs in 2 – 4 weeks, monitored by low Alk Phos, Rising Vit D and XR change