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PAEDS - MSK / DERMATOLOGY Flashcards

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1
Q

LIMP OVERVIEW
What is the main source of a limp?

A
  • Hip, then leg > knee > thigh > foot (least likely)
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2
Q

LIMP OVERVIEW
What are important differentials?

A

Intra-abdominal pathology like hernia, testicular torsion

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3
Q

LIMP OVERVIEW
What are some differentials for limp in a child 0–3y?

A
  • Trauma like # (accidental or NAI)
  • Infections (septic arthritis, osteomyelitis)
  • DDH (chronic)
  • Malignancy (Ewing’s, osteogenic sarcoma)
  • Neuromuscular disease (CP, Duchenne’s)
  • ANY CHILD <3Y WITH LIMP NEEDS URGENT ASSESSMENT*
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4
Q

LIMP OVERVIEW
What are some differentials for limp in a child 4–10y?

A
  • Trauma, infection, malignancy
  • Transient synovitis (acute)
  • Perthe’s disease (P for primary school, chronic)
  • Juvenile idiopathic arthritis (chronic)
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5
Q

LIMP OVERVIEW
What are some differentials for limp in a child >10y?

A
  • Trauma, infection, malignancy
  • Slipped upper femoral epiphysis (S for secondary school, acute/chronic)
  • JIA
  • Reactive arthritis
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6
Q

LIMP OVERVIEW
What are some general investigations for a child presenting with limp?

A
  • Full Hx + exam (top>toe)
  • General obs (HR, BP, temp)
  • FBC (WCC), CRP/ESR, blood cultures if septic
  • XR both AP + lateral for joint (+ joints above/below)
  • USS joint to look for thickening of capsule or effusion
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7
Q

DDH
What is developmental dysplasia of the hip (DDH)?

A
  • Abnormal relationship of femoral head to the acetabulum leading to aberrant development of hip causing instability
  • Spectrum of dysplasia (underdevelopment), subluxation (partial dislocation) or frank dislocation of the hip
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8
Q

DDH
What are some risk factors for DDH?
How would you manage them?

A
  • First degree FHx, breech at ≥36w or breech delivery ≥28w, multiple pregnancy
    – USS hip by 6w even if normal NIPE exam
  • Other = F>M 6:1, oligohydramnios
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9
Q

DDH
What is the clinical presentation of DDH?

A
  • Painless limp
  • Limited abduction (reduced ROM)
  • Leg length discrepancy
  • May have waddling or abnormal gait but otherwise well
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10
Q

DDH
What is the main investigation for DDH and what are you looking for?

A

NIPE at 72h + 6–8w

  • Leg length discrepancy
  • Restricted hip abduction of affected side
  • Barlow + ortolani tests
  • Clunking of hips on tests
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11
Q

DDH
What are you assessing for when you look at leg length discrepancy?

A

Galeazzi/Allis sign = difference in knee length when hips flexed + feet flat on bed

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12
Q

DDH
What are you assessing for when you look at barlow test?

A

Posterior hip dislocation (adduct hips + press down on knees)

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13
Q

DDH
What are you assessing for when you look at ortolani test?

A

Relocate a dislocated femoral head (abduct + push thigh anteriorly)

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14
Q

DDH
After the NIPE, what would be the investigation of choice if positive?
What other investigation might you perform?

A
  • USS by 2w of age
  • XR may be useful in older infants >3m
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15
Q

DDH
What is the management of DDH?

A
  • If <6m = Pavlik harness to hold femoral head in position (flexed + abducted) to allow the hip socket (acetabulum) to develop normal shape (remove after 6-8w)
  • Surgical reduction if harness fails or Dx >6m = hip spica cast to immobilise hip for prolonged period after surgery (risk of avascular necrosis + re-dislocation)
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16
Q

SEPTIC ARTHRITIS
What is septic arthritis?

A
  • Serious infection of the joint space as it can lead to bone destruction
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17
Q

SEPTIC ARTHRITIS
Who is it commonly seen in and how?

A
  • Most common <2y,
  • usually from haematogenous + soft tissue swelling
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18
Q

SEPTIC ARTHRITIS
What is the most common causative organism of septic arthritis?

A
  • Staphylococcus aureus
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19
Q

SEPTIC ARTHRITIS
What are common causes in…
i) infants?
ii) <4y?
iii) >4y?

A

i) GBS, S. aureus, coliforms
ii) S. aureus, pneumococcus, haemophilus
iii) S. aureus, gonococcus (adolescents)

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20
Q

SEPTIC ARTHRITIS
What is the clinical presentation of septic arthritis?

A
  • Usually single joint (knee or hip) + acute onset
  • Hot, red, swollen + painful joint (including at rest)
  • Refusal to weight bear
  • Stiffness + reduced ROM with pain if moved (hip may be held flexed)
  • Systemic = fever, lethargy, sepsis
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21
Q

SEPTIC ARTHRITIS
What are some investigations for septic arthritis?

A
  • FBC,
  • blood cultures,
  • CRP + ESR,
  • USS guided joint aspiration for MC&S
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22
Q

SEPTIC ARTHRITIS
what is the criteria for diagnosing septic arthritis?

A

Kocher’s modified criteria /5, ≥3 is likely
–Temp>38.5
– Raised CRP/ESR/WCC
– Non-weight bearing

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23
Q

SEPTIC ARTHRITIS
What is the management of septic arthritis?

A
  • IV empirical Abx (flucloxacillin) until sensitivities back
  • Arthroscopic lavage or surgical drainage if resolution does not occur rapidly or deep-seated joint (hip)
  • Immobilise joint initially but then mobilise to prevent deformity
  • Rest + analgesia
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24
Q

OSTEOMYELITIS
What is osteomyelitis?

A
  • Infection in the bone + bone marrow, often in the metaphysis of long bones
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25
OSTEOMYELITIS What are the two different types?
- Acute = rapid presentation with acutely unwell child - Chronic = deep seated, slow growing infection + Sx
26
OSTEOMYELITIS What causes osteomyelitis?
S. Aureus #1 or H. influenzae (directly via bone or haematogenous spreading)
27
OSTEOMYELITIS What is the epidemiology?
M>F, <10y
28
OSTEOMYELITIS What are some risk factors?
- Open #, - orthopaedic surgery, - sickle cell anaemia (Salmonella predominates), - immunocompromised (HIV),
29
OSTEOMYELITIS What is the clinical presentation of osteomyelitis?
- Acutely unwell child - Refusing to weight bear - Severe pain, swelling + tenderness - May have high fever (low grade if chronic)
30
OSTEOMYELITIS What are some investigations for osteomyelitis?
- FBC (Raised WCC), raised ESR/CRP, blood cultures, bone marrow aspiration MC&S - XR can be normal - MRI is best imaging to establish Dx
31
OSTEOMYELITIS What is the management of osteomyelitis?
- IV empirical Abx (flucloxacillin or clindamycin if allergy) until sensitivities back - Amoxicillin, cefotaxime or ceftriaxone if <4y + suspect H. influenzae - ?Surgical drainage or debridement of infected bone
32
PERTHE'S DISEASE What is the pathophysiology of Perthe's disease?
- Disruption of blood flow to femoral head causing avascular necrosis of the bone - Affects the epiphysis of femur, which is bone distal to growth plate (physis) - Over time, revascularisation or neovascularisation + healing of the femoral head with remodelling of bone
33
PERTHE'S DISEASE What are some risk factors for Perthe's disease?
- Social deprivation - LBW - Passive smoking
34
PERTHE'S DISEASE What is the clinical presentation of Perthe's disease?
- 4-8y, mostly male, limp (no Hx of trauma) - Pain (often unilateral) in hip or groin (?knee referral) with restricted hip movements (internal + external rotation) - +ve Trendelenburg test (abductor dysfunction) = 'sound side sags'
35
PERTHE'S DISEASE What are the investigations for Perthe's disease?
- Blood tests all normal - XR of both hips (with frog views) is initial investigation + assesses healing – Flattening of femoral head - Technetium bone scan or MRI may be needed to confirm Dx if normal XR
36
PERTHE'S DISEASE What are the complications of Perthe's disease?
- Premature fusion of the growth plates - Soft + deformed femoral head can lead to early hip OA
37
PERTHE'S DISEASE What is the general management of Perthe's disease?
- Keep femoral head within acetabulum (cast, braces) - Physio to retain ROM in muscles + joints without excess stress on the bone
38
PERTHE'S DISEASE What is the management of Perthe's disease for... i) <6y + less severe? ii) older, severe or not healing?
i) Conservative + observe, bed rest, traction, crutches, analgesia (good prognosis) ii) Surgery to improve alignment + function of the femoral head + hip
39
JIA What is juvenile idiopathic arthritis (JIA)?
- Autoimmune inflammation in joints > joint pain, swelling + stiffness
40
JIA What is the criteria for a clinical diagnosis of JIA?
- Onset before 16y with no underlying cause - Joint swelling/stiffness - >6w in duration to exclude other causes (i.e. reactive)
41
JIA What is the clinical presentation of JIA?
- Joint pain, swelling + stiffness (particularly morning) = hallmarks - Limping/functional disability - Decreased ROM - Warmth + colour change
42
JIA What are the 4 types of JIA?
- Systemic JIA (Still's disease) - Polyarticular JIA - Oligoarticular JIA - Enthesitis-related arthritis
43
JIA How does systemic JIA (Still's disease) present?
- Subtle salmon-pink rash - High swinging fevers - Lymphadenopathy, weight loss, muscle pain, splenomegaly - Pleuritis, pericarditis + uveitis
44
JIA What are the investigations for systemic JIA?
- Antinuclear antibodies (ANA) + rheumatoid factor = NEGATIVE - Raised inflammatory markers = CRP/ESR, platelets + serum ferritin
45
JIA What is the main complication of systemic JIA?
- Macrophage activation syndrome = severe activation of immune system with massive inflammatory response
46
JIA How does macrophage activation syndrome present?
- Acutely unwell with DIC, - febrile, - anaemia, - thrombocytopenia, - bleeding, - non-blanching rash, - low ESR
47
JIA What is the management of macrophage activation syndrome?
Life-threatening = supportive + steroids
48
JIA What is polyarticular JIA?
- ≥5 joints affected, equivalent of RA in adults
49
JIA What are the features of polyarticular JIA?
Symmetrical, affects small joints (of hand + feet) as well as large joints (hips + knees)
50
JIA How does polyarticular JIA present?
Mild systemic Sx = mild fever, anaemia + reduced growth
51
JIA What is the immunology of polyarticular JIA?
If rheumatoid factor +ve = seropositive (tend to be older children)
52
JIA What is oligoarticular JIA?
≤4 joints affected, often just monoarthritis
53
JIA What is oligoarticular JIA classically associated with?
Anterior uveitis = ophthalmologist referral
54
JIA what is the immunology of oligoarticular JIA?
ANA +ve but RF -ve
55
JIA What is enthesitis-relataed arthritis?
- Paeds version of seronegative spondyloarthropathies (ankylosing spondylitis, psoriatic/reactive arthritis, IBD-related arthritis)
56
JIA What is the main feature?
Enthesitis = inflammation at the point a tendon or muscle inserts to bone
57
JIA How might enthesitis-related arthritis present?
- Sx of psoriasis (psoriatic plaques, nail pitting, dactylitis) or IBD
58
JIA What is it associated with?
- HLA-B27 gene - Prone to anterior uveitis = ophthalmology referral
59
JIA What is reactive arthritis?
- Arthritis that develops following an infection where the organism cannot be recovered from the joint
60
JIA What causes reactive arthritis?
Post STI (chlamydia) in older children or Salmonella, Campylobacter
61
JIA How does reactive arthritis present?
- Reiter's = can't see (conjunctivitis), can't pee (urethritis) and can't climb a tree (arthritis)
62
JIA What is the general management?
Sx (analgesia, NSAIDs, sometimes intra-articular steroids)
63
JIA What are the XR features of JIA?
Same as RA (LESS) – - Loss of joint space - Erosions (causing joint deformity) - Soft tissue swelling - Soft bones (osteopenia)
64
JIA What are some complications from JIA?
- Chronic anterior uveitis > severe visual impairment - Flexion contractures of joints - Growth failure + constitutional problems like delayed puberty - Osteoporosis
65
JIA What is the non-medical management of JIA?
- MDT approach = education, psychologist, physio, pain team, rheumatology
66
JIA What is the medical management of JIA?
- NSAIDs for Sx relief during flares - Intra-articular steroids for oligoarthritis - Avoid systemic steroids if possible (osteoporosis, growth suppression) – IV methylprednisolone can be used if severe arthritis - DMARDs like methotrexate, rarely sulfasalazine for polyarthritis - Biologics if poor control like tocilizumab, adalimumab, etanercept
67
TRANSIENT SYNOVITIS What is transient synovitis?
- 'Irritable hip' caused by transient inflammation of the joint synovial membrane
68
TRANSIENT SYNOVITIS What is it associated with?
Recent viral URTI, small % will develop Perthe's
69
TRANSIENT SYNOVITIS What is the clinical presentation of transient synovitis?
- Limp + refusal to weight bear, 2–10y - Groin or hip pain (may be referred to knee) - Mild low-grade fever but otherwise systemically well - Limited internal rotation + pain on movement but comfortable at rest
70
TRANSIENT SYNOVITIS What are some investigations for transient synovitis?
- #1 = exclude septic arthritis so if suspect = cultures + joint aspiration - Normal WCC, slight increase in CRP - USS may show effusion but XR normal
71
TRANSIENT SYNOVITIS What is the management of transient synovitis?
- Self-limiting with only simple analgesia + rest = rapid Sx improvement - Manage at home with safety netting + review to ensure no fever + Sx resolving
72
SUFE/SCFE What is slipped upper/capital femoral epiphysis? (SUFE/SCFE)?
- Displacement of femoral head epiphysis postero-inferiorly along the growth plate (through zone of hypertrophy)
73
SUFE/SCFE What is SUFE/SCFE associated with?
- Boys, >10y, obese + undergoing growth spurt - Metabolic endocrine abnormalities (hypothyroid)
74
SUFE/SCFE What is the clinical presentation of SUFE/SCFE?
- May be Hx of minor trauma that triggers onset - Hip, groin, thigh or knee pain (disproportionate to severity of trauma) - Painful limp + may have antalgic gait - Very restricted internal rotation (+ abduction)
75
SUFE/SCFE What are the investigations for SUFE/SCFE?
- XR initial Ix of choice (AP + frog-leg views) - Bloods (incl. inflammatory markers) normal - ?Technetium bone scan + MRI scan
76
SUFE/SCFE What is the management of SUFE/SCFE?
- Surgery = internal fixation (pinning femoral head into position for prevention)
77
OSGOOD SCHLATTERS What is Osgood-Schlatters disease? What is the epidemiology?
- Inflammation at the tibial tuberosity where the patellar ligament inserts - 10–15y sporty males (football, basketball)
78
OSGOOD SCHLATTERS What is the clinical presentation of Osgood-Schlatters disease?
- Visible or palpable hard + tender lump/swelling at tibial tuberosity - Pain in anterior aspect of knee, often unilateral - Exacerbated by physical activity, kneeling + extension of knee
79
OSGOOD SCHLATTERS What is the management of Osgood-Schlatters disease?
- Reduce pain + inflammation = NSAIDs, ice, reduce exercise) - Stretching + physio once settled to strengthen joint + improve function
80
GROWING PAINS What are growing pains?
Diagnosis by exclusion – - Pain never present at start of day after waking but can awaken from sleep - Physical activities are not limited, no limp, settles with massage - Bilateral pain in lower limbs (shins/ankles) + not limited to joints - Can be worse after a day of vigorous activity + intermittent
81
OSTEOPOROSIS What is osteoporosis in paediatrics defined by?
- ≥1 vertebral crush # - ≥2 long bone fractures by age 10 (≥3 by age 19) - Bone mineral density less than 2.5 standard deviations below the mean
82
OSTEOPOROSIS How would you investigate?
- Bone mineral density less than 2.5 standard deviations below the mean - DEXA scan
83
OSTEOPOROSIS What are the causes of osteoporosis?
- Inherited = osteogenesis imperfecta, haematological issues - Acquired: – Drug induced (Steroids) – Endocrinopathies (hypoparathyroidism) – Malabsorption – Immobilisation (disabilities) – Inflammatory disorders
84
OSTEOGENESIS IMPERFECTA What is osteogenesis imperfecta?
- Autosomal dominant condition leading to brittle bones + prone to fractures
85
OSTEOGENESIS IMPERFECTA What is the pathophysiology?
Defects in type 1 collagen protein which is essential for the structure + function of bone, as well as skin, tendons + other connective tissues
86
OSTEOGENESIS IMPERFECTA What is the clinical presentation of osteogenesis imperfecta?
- Bone fragility = recurrent + inappropriate #, joint + bone pain - Bone deformity (bowed legs, bent bones, scoliosis) - Impaired mobility due to poor muscle mass - Poor growth > short stature - Hypermobility as ligamentous laxity
87
OSTEOGENESIS IMPERFECTA What are some associations with osteogenesis imperfecta?
- Conductive hearing loss (otosclerosis) - Blue/grey tinted sclera due to scleral thinness - Valvular prolapse, aortic dissection > aortic incompetence - Hernias - 'Wormian bones' = skull feels like bubble wrap (wiggly black lines on skull XR)
88
OSTEOGENESIS IMPERFECTA What are the investigations for osteogenesis imperfecta?
- Clinical Dx with XR to diagnose fractures + bone deformities - DEXA scan to look at bone mineral density (osteoporosis) - 7 types under the sillence classification
89
OSTEOGENESIS IMPERFECTA In the Sillence classification, what is... i) type 1? ii) type 2? iii) types 3–4?
i) Mildest form, common with blue sclera ii) Lethal form, chest too small to allow breathing, lots of rib # + lungs do not function iii) Normal sclera
90
OSTEOGENESIS IMPERFECTA What is the MDT management of osteogenesis imperfecta?
- Physio + OT to maximise strength + function - Paeds for medical treatment + follow up - Orthopaedic surgeons to manage # - Pain team, specialist nurses for advice + support
91
OSTEOGENESIS IMPERFECTA What is the medical management of osteogenesis imperfecta?
- Vitamin D supplementation to prevent deficiency - Bisphosphonates (IV pamidronate) to increase bone density + reduce #
92
RICKETS What is rickets? What is it caused by?
- Defective bone mineralisation > "soft" + deformed bones (paeds osteomalacia) - Vitamin D deficiency (recommended paeds intake 400IU = 10mg)
93
RICKETS What are some risk factors for rickets?
- Darker skin (need more sunlight) - Lack of exposure to sun - Poor diet or malabsorption - CKD as kidneys metabolise vitamin D to active form
94
RICKETS What is the normal physiology of vitamin D?
- Increases Ca2+ absorption at gut + reabsorption at kidneys + role in immunity
95
RICKETS What are some sources of vitamin D?
Sunlight, fortified cereals, eggs, oily fish
96
RICKETS What happens when there is inadequate vitamin D?
- Lack of Ca2+ + phosphate in blood which are required for bone construction > defective bone mineralisation - Low Ca2+ causes secondary hypoparathyroidism as parathyroid gland tries to raise Ca2+ level by secreting parathyroid hormone - This leads to increased resorption of Ca2+ from the bones, worsening the issue
97
RICKETS What are the symptoms of rickets?
- Bone pain, swelling + deformities - Muscle weakness + poor growth (gross motor delay) - Pathological or abnormal # - May have hypocalcaemic convulsions or carpopedal spasm
98
RICKETS What are some bone deformities seen in rickets?
- Bowing of legs, knock knees - Harrison sulcus = indentation of softened lower ribcage at site of attachment of diaphragm - Rachitic rosary = ends of ribs expand at costochondral junctions causing lumps along chest - Craniotabes = soft skull with delayed closure of sutures + frontal bossing - Expansion of metaphyses (esp. wrist)
99
RICKETS What are some investigations for rickets?
- Serum biochemistry - FBC + ferritin (Fe anaemia), inflammatory markers - Kidney, liver + TFTs, malabsorption screen (anti-TTG) - Autoimmune + rheumatoid tests - XR required to diagnose
100
RICKETS What would serum biochemistry show in rickets?
- Low = calcium + phosphate - High = ALP + PTH - 25-hydroxyvitamin D levels deficient (<25nmol/L)
101
RICKETS What might an XR show in rickets?
- Osteopenia (radiolucent bones) - Cupping - Fraying of metaphyses - Widened epiphyseal plate
102
RICKETS What is the management of rickets?
Prevention #1 – - Breastfeeding women should take vitamin D supplement - Dietary advice to increase calcium + vitamin D - Children vitamin D deficient > ergocalciferol Vitamin D + calcium supplementation for children with rickets + specialist input
103
COMMON BIRTHMARKS What is a salmon patch?
- 'Stork mark' - Most common vascular birthmark - Flat red or pink patches on baby's eyelids, neck or forehead at birth - Fade completely in few months
104
COMMON BIRTHMARKS What is a cavernous haemangioma?
- 'Strawberry mark' - Raised marks on skin often red, F>M - Not present at birth, appear in first month, increase in size then shrink + disappear - Normally self-limiting, beware over eye + airway
105
COMMON BIRTHMARKS What is a capillary haemangioma?
- 'Port wine stain' = permanent, often unilateral - Present at birth + grows with infant, treated with laser therapy - Seen in Sturge-Weber syndrome (neuro Sx)
106
COMMON BIRTHMARKS What is a naevi?
- Mole, can be multiple present in Turner's
107
COMMON BIRTHMARKS What is a slate grey naevi? What are the differentials for slate grey naevi?
- Mole, can be multiple present in Turner's - 'Mongolian blue spot', disappear by 4, commonly lower back/buttocks, more common in non-Caucasian - Bruising + NAI so important to document
108
COMMON BIRTHMARKS What are café-au-lait spots? What is the significance?
- Flat, light brown patches on skin - >5 = neurofibromatosis
109
COMMON BIRTHMARKS What are milia?
Milk spots (sebaceous plugs where sweat glands plugged by sebum), normal
110
COMMON BIRTHMARKS What are infantile urticaria?
Erythema toxicum neonatorum by histamine reaction = self-limiting red blotches with eosinophils on biopsy
111
ECZEMA What is eczema?
- Chronic atopic condition caused by defects in normal continuity of skin barrier leaving tiny gaps for irritants, microbes + allergens to enter + trigger immune response - Leads to inflammation of the skin
112
ECZEMA What is the clinical presentation of eczema?
- Infants = dry, red, itchy + sore patches of skin over face + trunk - Young children = extensor surfaces - Older children = mostly on flexor surfaces (creases), face + neck creases
113
ECZEMA What are some complications of eczema?
- Opportunistic bacterial infection as skin breakdown leaves entry, particularly S. aureus – Presents as increased erythema, yellow crust, pustules – PO flucloxacillin or admit for IV if severe - Eczema herpeticum
114
ECZEMA What is the general management of eczema?
- Avoid triggers (weather, stress, wash/cleaning products) - Maintenance = artificial skin barrier with emollients (E45), special soap substitutes
115
ECZEMA How should a flare of eczema be managed?
- Thicker emollients (hydromol or epaderm) - Topical steroids (start with hydrocortisone > betnovate > dermovate) - Wet wraps = cover affected areas in thick emollient with wrap to keep moisture overnight - Severe = PO ciclosporin, corticosteroids
116
ECZEMA What are some side effects of using topical steroids?
- Thinning of skin - Telangiectasia - Bruising
117
PSORIASIS What is the pathophysiology of psoriasis?
- Chronic autoimmune condition where abnormal T-cell activation > hyperproliferation of keratinocytes + so psoriatic skin lesions
118
PSORIASIS What are the causes?
- HLA-B13, - environmental triggers (alcohol, stress, group A strep)
119
PSORIASIS What are the different types of psoriasis?
- Plaque - Guttate 'rain-drop' - Erythrodermic + pustular
120
PSORIASIS How does plaque psoriasis present?
- Well-demarcated, raised, silvery scaling lesions on extensor surfaces (elbows + knees) - Scalp involvement, most often at hair margin
121
PSORIASIS How does guttate psoriasis present?
- Explosive eruption of very small circular plaques on trunk, often 2w after strep throat - Common in paeds, resolves in 3-4m
122
PSORIASIS How does erythrodermic + pustular present?
- Most severe + life-threatening - Widespread inflammation of skin > extensive erythematous areas or pustules under areas of erythema - Systemic = pyrexia, malaise - Admit
123
PSORIASIS What is the clinical presentation of psoarisis?
- Koebner phenomenon = new plaques of psoriasis at sites of skin trauma - Residual pigmentation of skin after lesions resolve - Auspitz sign = small points of bleeding when plaques scraped off - Nail changes (pitting + onycholysis)
124
PSORIASIS What are some associations of psoriasis?
- 10–20% develop psoriatic arthritis - Increased risk of CVD, metabolic syndrome, VTE
125
PSORIASIS What is the management of psoriasis?
- 1st line = topical steroids, topical vitamin d analogues (calcipotriol) - 2nd line = UV phototherapy - 3rd line = immunosuppression with methotrexate or biologics
126
NAPPY RASH What are the 2 main types of nappy rash?
- Irritant dermatitis = friction between skin/nappy + contact with urine + faeces - Candida dermatitis = due to breakdown in skin + the warm, moist environment
127
NAPPY RASH How do you differentiate between irritant dermatitis and candida dermatitis?
- Irritant = sore, red, inflamed skin but spares the skin creases - Candida = involves skin creases, satellite lesions (small similar lesions near edges of principle lesion) + may have oral thrush
128
NAPPY RASH What are some risk factors for developing nappy rash?
- Delayed changing of nappies - Diarrhoea - Irritant soap products + vigorous cleaning - PO Abx predispose to Candida
129
NAPPY RASH What is the management of nappy rash?
- Highly absorbent nappies - Maximise time not wearing + ensure dry before replacing nappy - Change nappy + clean skin ASAP - Water or gentle alcohol-free products to clean - Topical imidazole if candida
130
STEVEN-JOHNSON What is Steven-Johnson syndrome? What versions are there?
- Disproportional immune response causes epidermal necrosis > blistering + shedding of top layer of skin - SJS = <10% body surface, toxic epidermal necrolysis affects >10%
131
STEVEN-JOHNSON What are some potential causes of Steven-Johnson syndrome?
- Meds = AEDs, Abx, allopurinol, NSAIDs - Infections = herpes simplex, mycoplasma pneumonia, CMV, HIV
132
STEVEN-JOHNSON What is the clinical presentation of Steven-Johnson syndrome?
- Non-specific Sx of fever, cough, sore throat + itchy skin - Develop purple/red rash that spreads across skin, starts to blister - Few days later skin sheds leaving raw tissue underneath = PAINFUL
133
STEVEN-JOHNSON Where does it affect?
- Non-specific Sx of fever, cough, sore throat + itchy skin - Develop purple/red rash that spreads across skin, starts to blister - Few days later skin sheds leaving raw tissue underneath = PAINFUL - Can involve lips + mucous membranes, urinary tract, lungs - Eyes can become inflamed + ulcerated
134
STEVEN-JOHNSON What are some complications of Steven-Johnson syndrome?
- Secondary infection - Permanent skin damage due to skin involvement + scarring - Visual complications such as severe scarring or even blindness
135
STEVEN-JOHNSON What is the management of Steven-Johnson syndrome?
- Admission as medical emergency, cease causative meds - Nutritional care, Abx, analgesia, ophthalmology input - Steroids, immunoglobulins + immunosuppressants by specialists
136
DISCOID MENISCUS what is it?
- it is an abnormally shaped meniscus (usually lateral) - it usually presents in younger people - it is more prone to injury as it is more likely to get stuck/tear
137
DISCOID MENISCUS how does it present?
- a visible or audible snap on terminal leg extension along with pain and swelling in the absence of trauma
138
DISCOID MENISCUS what are the investigations?
- MRI - can show abnormal shape and any tears - clinical examination
139
DISCOID MENISCUS what is the management?
- symptomatic = arthroscopic partial meniscectomy - asymptomatic = physiotherapy
140
SCOLIOSIS what is it?
it is lateral curvature in the frontal plane of the spine - measured >10 degrees on x-ray
141
SCOLIOSIS what are the causes?
- idiopathic = most common - congenital = usually from congenital structural defect of the spine e.g. spina bifida - secondary = neuromuscular imbalance (cerebral palsy, muscular dystrophy), disorders of bone or connective tissues
142
SCOLIOSIS what is the clinical presentation?
- visible curve in spine - shoulders, waist or hips look uneven - one shoulder blade appears bigger - ribs stick out further on one side - low back pain - back stiffness - pain + numbness in legs - fatigue (due to muscle strain)
143
SCOLIOSIS what conditions can cause scoliosis?
cerebral palsy muscular dystrophy birth defects infections tumours marfan syndrome down syndrome
144
SCOLIOSIS what is the management?
- braces - spinal fusion surgery - spine and rib-based growing operation
145
TORTICOLLIS what is it?
- tilting of the head to one side caused by contraction of the neck muscles
146
TORTICOLLIS what are the different types?
- congenital - acquired
147
TORTICOLLIS what are the causes of congenital torticollis?
- congenital muscular torticollis (CMT) = usually noticed in 1st month after birth. It causes shortening + fibrosis of sternocleidomastoid (can have palpable mass) - malformed cervical spine - spina bifida
148
TORTICOLLIS what are the causes of acquired torticollis?
- MSK = muscle spasm - infection = URTI, otitis media, dental infection, pharyngeal infection - atlantoaxial rotatory fixation - inflammation = juvenile idiopathic arthritis - neoplasm = CNS tumours
149
TORTICOLLIS how does it present?
- awkward head posture for a prolonged time
150
TORTICOLLIS what are the investigations?
most of the time it is a clinical diagnosis - cervical spine x-ray can be useful
151
TORTICOLLIS what is the management?
treat the cause - muscle spasm = self resolve - infection = antibiotics - Congenital = physiotherapy
152
OSGOOD SCHLATTERS what is it?
it is an overuse injury that is common in skeletally immature athletic young people it occurs secondary to repetitive activities such as jumping, sprinting etc.
153
OSGOOD SCHLATTERS when does it usually develop?
during the stage of bone maturation 10-12 in girls 12-14 in boys
154
OSGOOD SCHLATTERS what is the cause?
repeated traction over the tibial tubercle which results in microvascular tears, fractures and inflammation
155
OSGOOD SCHLATTERS what are the risk factors?
- male gender - age - 12-15 in boys, 8-12 in girls - sudden skeletal growth - repetitive activities such as jumping and sprinting
156
OSGOOD SCHLATTERS what is the clinical examination?
- anterior knee pain with or without swelling - pain aggravated by physical activity
157
OSGOOD SCHLATTERS what are the investigations?
clinical diagnosis
158
OSGOOD SCHLATTERS what is the management?
- conservative treatment - RICE - surgical treatment in severe cases once the child has fully grown - physiotherapy

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