Orthopaedics Flashcards
DDH, limp, osteomyelitis, septic arthritis, transient synovitis, rickets, JIA, Perthe's disease, reactive arthritis
Bow legs + knock knees
Bow legs (genu varum): knees wide, common when first walk normal up to 3y but may be path in rickets or Blount disease
Knock knees (genu valgum): feet wide knees close, common in young + usually goes spontaneously
Flat feet (pes planus)
Usually disappears
May persist in hypermobility, contractures or JIA
In-toeing
Common, child can fall, normally self-limiting
Metatarsus varus: adduction deformity, passively correctable
Medial tibial torsion: tibia LR less than normal, self corrects by 5y
Persistent ante version of femoral neck: femoral neck twisted more than normal at hip, usually goes by 8y, may be a/w hypermobility
Toe walking
Common in young children, may persist with habit or DMD/tight achilles tendon/cerebral palsy/inflammatory arhtritis
Developmental dysplasia of the hip
A spectrum from dysplasia - subluxation - frank dislocation
RF: breech, female (6x), FH, first born, oligohydramnios, macrosomic bw, congenital calcaneovalgus foot deformity
Screened for in NIPE, at 8w check, hip US to confirm. Do hip US on infants who have RF for it (not XR as hip not calcified) as the screening signs can be missed
Later presentation: limp, abnormal gait, asymmetrical skin folds around hip, limited abduction, shortening of affected leg
M: if just unstable most stabilise by 6w, Pavlik harness in up to 4-5 months old (keeps hip flexed + abducted, for up to 6m), surgery if fails/identified late
Comp: necrosis of femoral head
Causes of limp in young child (1-3y)
- Acute: SA, OM, transient synovitis, trauma, malignancy (neuroblastoma, leukaemia)
- Chronic: DDH, talipes, cerebral palsy, JIA
Causes of limp in older child (3-10y)
- Acute: transient synovitis, SA, OM, trauma/overuse, Perthes disease, JIA, leukaemia, complex regional pain syndrome
- Chronic: Perthes, DMD, JIA, tarsal coalition
Causes of limp in adolescents
- Acute: trauma/overuse, SUFE, AVN of FH, reactive arthritis, JIA, SA/OM, osteochondritis dissecans (knee), bone tumours, complex regional pain syndrome
- Chronic: chronic SUFE, JIA, tarsal coalition
Osteomyelitis
This is infection of the metaphysis of long bones (often distal femur/proximal tibia); 15% also have SA
Path: haematogenous spread (or direct spread from wound), S aureus commonest, Strep, H influenza if not immunised; in SCD also at risk of salmonella (but Staph is still commonest)
CF: markedly painful immobile limb + acute febrile illness, may have a sterile effusion of an adjacent joint, back/groin pain if vertebral/pelvic bones, infants may be more insidious
Ix: BC+, WCC + CRP raised, XR may be initially normal, US-periosteal elevation, MRI-subperiosteal pus + purulent debris in bone
M: IV Abx for weeks until clinically recovered, then oral Abx for several weeks; may need surgical decompression/drainage
Comps: necrosis, chronic infection (discharging sinus, deformity)
Rickets causes
Failure of mineralisation in growing bone/osteoid tissue
- nutritional (primary): insufficient exposure to direct sun, dark skin means less absorption, maternal vitamin D def, diets low in calcium/phosohorous/vit D (e.g. prolonged ebf, vegans)
- intestinal malabsorption e.g. coeliac, pancreatic insufficiency in CF, high phytic acids in diet e.g. chapattis
- defective 25-hydroxyvitamin D production in chronic liver disease
- increased 25-hydroxyvitamin D metabolism via enzyme induction from AEDs
- defective production of 1,25-dihydroxyvitamin D in CKD, Fanconi syndrome
Rickets CF
Craniotabes-press over occipital/parietal bones feels like pressing a ping pong ball Rachitic rosary - palpable costochondral junctions Widened wrists/ankles esp in crawling infants Harrisons sulcus cos ribs softened Bow legs Misery Poor growth Delayed closure of anterior fontanelle Hypotonia Seizures Cardiomyopathy Flattened skull Dental disease
Bloods: low/normal calcium, low phosphate, high ALP, low/normal 25-hydroxyvitamin D, high PTH
XR wrist: cupping + fraying of metaphases, widened epiphyseal plate
Rickets management
Nutrition - balanced diet with oily fish/egg yolk/milk/cereals/fruit juice; plus supplements vit D3 (cholecalciferol)
Correct RF
Healing 2-4w
Septic arthritis
Joint space infection can cause joint destruction, haematogenous or from OM spreading/puncture wound/skin lesions
Usually affects one joint-mostly hip in young children
Most commonly due to S aureus (used to be Hib but now vaccine), consider immunodeficiency or sickle cell
CF: red warm tender joint, reduced ROM, acutely unwell febrile child, infants often hold limb still (hardest to diagnose in them cos more SC fat), joint effusion in neighbouring joints, may have referred pain to knee
Ix: high WCC + CRP, take BC, US-effusion, XR-exclude trauma (SA initially normal but may have widened joint space/ST swelling), MRI/isotope scan if site of infection unclear; definitive = aspiration of joint space under US (For culture; ideally do immediately)
M: IV Abx then prolonged oral course, wash out/drainage if deep e.g. hip or unresponsive, immobilisation initially then mobilise to prevent deformity
Causes of a swollen joint
- Infection - SA, OM
- Inflammation - JIA, reactive arthritis, HSP, IBD, serum sickness (type 3 hypersensitivity reaction from an injection, usually also rash)
- Acute joint bleed - haemophilia
- Malignancy - leukaemia, neuroblastoma
- Trauma
Transient synovitis
Commonest cause of acute hip pain in 2-12y, often follows/accompanies a viral infection
Diagnosis of exclusion - usually still do BC + aspiration
CF: sudden onset pain in hip/limp, no rest pain, reduced ROM, may be referred to knee, afebrile/mild fever + not unwell
M: bed rest, usually improves in a few days
Juvenile idiopathic arthritis
Persistent joint swelling >6w in absence of infection or any other cause
Majority distinct from RA, at least 7 subtypes (based on which joints initially affected, HLA type + extra CF)
CF: gelling, morning joint stiffness, pain, younger kids may be intermittent limp/deterioration of behaviour/activities rather than pain complaints, usually develop swelling from fluid/inflam/synovial proliferation/peri-articular swelling
Ix: often initially clear, anti-nuclear factor may be + (but can be + in unaffected!)
Differential: widespread joint pain + fatigue consider a CT disorder
Comps: chronic anterior uveitis (can result in glaucoma/cataracts), flexion joint contractures, growth failure (generalised from steroids/anorexia, or localised like leg length discrepancy), constitutional e.g. anaemia of chronic disease, osteoporosis
M: induce remission ASAP, NSAIDs for analgesia, steroid joint injections (v good if oligoarticular, usually sedation/Entonox), methotrexate (weekly tablet/injection, good for poly arthritis, need regular bloods, nausea common), systemic steroids (avoid as much as poss), cytokine modulators (when refractory to methotrexate, strict guidance as spenny)
Growing pains
Common in 3-12y, not actually due to growth, something like ‘benign idiopathic nocturnal limb pains of childhood’
Features: never present on waking, no limp, no limitation of activities, systemically well, normal examination, motor milestones reached, often intermittent, often worse after a day of lots of activity
Perthe’s disease
This is AVN of femoral capital epiphysis due to interrupted blood supply then re-vascularisation + re-ossification occurs
M>F, most 5-10y
CF: insidious limp, hip/knee pain, usually u/l
Ix: XR inc frog views show increased density or irregularity of femoral head
M: rest, physio to optimise movement, some cases traction/casting/surgery to contain FH within acetabulum
Most good prognosis, if older/worse involvement of epiphysis may get deformity of FH/metaphyseal damage so more chance of OA
Reactive arthritis
Acute arthritis
CF: transient joint swelling <6w, often ankles/knees, usually a h/o another infection (usually enteric like Salmonella/Shigella/Campylobacter; or could be viral; or STIs in adolescents; or Lyme disease), low grade fever
Ix: acute phase reactants normal/slightly raised, XR normal
M: just NSAIDs for pain, complete recovery
Scoliosis
Lateral curvature in frontal plane of spine, rotation of vertebral bodies causes a prominence in back from rib asymmetry
most are mild but severe can cause cardio-rest issues
severe may need bracing/surgery
causes: idiopathic (most, onset in puberty), congenital (structural defects like VACTERL association or spina bifida), secondary to other disorders (e.g. CP, muscular dystrophy)
Torticollis
‘Wry neck’
Causes: SCM tumour (congenital), muscular spasm, ENT infection, spinal tumour, cervical spine arthritis etc
Causes of anterior knee pain in adolescents (most due to growth spurt so more pressure + most self resolve)
- chondromalacia patellae - softened articular cartilage in patella, if crepitus can do arthroscopy to smooth
- lateral pressure syndrome - lateral pain
- synovial shelf syndrome (plica) - synovial irritation from trauma/pressure
- jumper’s knee - at insertion of patellar tendon onto lower pole of patella, can try hydrocortisone injection at site of pain (not the tendon)
- bipartite patella - separate fragment of patella, usually leave
Foot deformities
Forefoot deformities - commonest
Club foot (talipes equinovarus): seen at birth, or postural development. both feet turned in, PF of ankle, inversion of foot, adducted forefoot. need serial plaster casts to prevent bony deformity. ponseti treatment
Slipped upper femoral epiphyses
Emergency
Typical pt is a chubby or lanky teenage boy
CF: groin/knee pain, limp, when sit w legs dangling sole of affected leg points towards other foot, limited hip movement
M: surgery to pin FH back into place to prevent AVN + OA
Osgood-Schlatter disease
Osteochondritis of the tibial tubercle - in teenagers w persistent pain over tibial tubercle, worsened by quadricep contraction, no knee swelling, RICE usually helps
Paediatric fractures usually heal well, potentially problematic ones?
- supracondylar humerus #: risk of Volkmann ischaemic contracture (brachial artery injury) or nerve damage e.g. anterior interosseous branch of median n, monitor for compartment syndrome
- lateral condyle #: tendency to displace
- growth plate #
Types of # particularly seen in kids?
Greenstick #: unilateral cortical breach only, may be angulated so needing reduction, plastic deformity on side of impact interrupted on opposite side
Plastic deformity: deformity without cortical disruption
Torus/buckle: incomplete cortical disruption causing periosteal haematoma only, doesn’t need fixing, from compression
Toddlers #: oblique tibial # in infants
Complete #: when both sides of cortex breached
Physeal #: more likely during growth spurts
What are the differences in paediatric # compared to adults?
- anatomical: different bony proportions, epiphyses, apophyses (trochanters, tibial tuberosity)
- biomechanical: ligaments stronger than GP so easier to break epiphyses but harder to dislocate, more elastic bones
- physiological: heals 2x faster, non-union rare
Osteogenesis imperfecta
Disorder of type I collagen synthesis, often sporadic but can be inherited - don’t form enough osteoid
CF: bowing, fracture prone, discoloured thick teeth, blueish sclera (due to abnormal sclera so see retinal pigmentation)
XR: translucent bones, multiple #, wormian bones (irregular patches of ossification)
M: IV pamidronate to reduce #, surgical implants/osteotomies
How are fractures described?
By mechanism: direct blow, indirect like twisting, pathological (abnormal weakness of the bone), fatigue # (e.g. toe # from walking too much)
Open (open wound) vs closed
By shape: transverse (bones more aligned), spiral (twisting, most long bone #), oblique (blow e.g. protecting face in a fight, usually actually spiral as true obliques are rare), comminuted (bone splintered), crush (cancellous bone squashed, have to pack space with bone graft/external fixation)
Displaced - fragments not in anatomical position so need reduction; undisplayed - fragment nearly in anatomical position
Stable - unlikely to move
Salter-Harris fracture classification for growth plate #
Slipped (type 1: babies/pathological, # along the epiphyseal line)
Above (type 2: commonest, # above the growth plate)
Lower (type 3: # of the epiphysis with part of it still attached to shaft)
Through (type 4: through epiphysis + shaft, union may interfere with growth)
Ruined (type 5: crushing injury, deformity + stunting)
Outline the stages of # healing
- Inflammation: haematoma, inflammatory cells, fibroblasts make granulation tissue, osteoblasts proliferate (NSAIDs represses this stage)
- Repair: primary callus within 2w (if bones not touching get bridging soft callus), endochondral ossification converts it to hard callus, cartilage produced then bone
- Remodelling: continues long after clinical union, most effective in children + nearer growth plate + in plane of normal movement
Complications of fractures
- Immediate: haemorrhage, artery damage, nerve damage, damage to structures like pneumothorax from rib #
- Early (weeks): infection, fat embolism (patchy consolidation, low plt, raised lipase, tachypnoea, petechiae, uncommon), chest infection, DIC, compartment syndrome
- Late: malunion (wrong position, may not be an issue), delayed union, non-union (serious esp if weight bearing), deformity, OA (in same or other joint if there was malunion), AVN (often takes ~2y to develop), traumatic chondromalacia (esp patella - articular cartilage softens - pain + crepitus)
Management principles of fractures
- Reduce - restore anatomical alignment, closed in emergency, or with immobilisation in a cast if not very displaced/openly ‘ORIF’
- Hold - traction in some # if muscle pull strong, simple splints, plaster casts (in first 2w not whole way around to allow swelling + prevent compartment syndrome), if axial instability (# can rotate along axis) cast needs to cross joint above + below
- Rehabilitate - PT, move non-mobilised joints
Radiological features of bone tumours
new bone/bone destruction cortex abnormalities widened medullary cavity periosteum lifted off bone onion skin appearance - Ewing's sarcoma sun ray radial calcification - osteogenic sarcoma
What hormones + vitamins affect bone growth?
GH: until epiphyses close
Testosterone: causes increase in growth then epiphyseal closure
Thyroid hormones: permits normal growth (low=growth stunted, high=osteoporosis)
PTH: mobilises calcium from bone + increases tubular calcium resorption
Vit C: collagen synthesis, needed for osteoid
Vit D: absorbs calcium from gut, affects muscle tone + bone absorption
Calcitonin: screed if serum calcium too high
Osteopetrosis
Marble bone disease, looks solid but actually v brittle
Autosomal recessive
May get anaemia/low plt due to reduce BM space
Achondroplasia
Autosomal dominant
Long bones dont grow as much as normal, short stature, normal strength, normal intelligence
Can get spinal stenosis from narrow spinal canal
Osteochondritis
Generic term for conditions that appear similar - bad term tbh
- vascular abnormalities like partial venous occlusions, perthes
- traction apophysitis from muscle pulling in growth spurt: Sinding Larsen disease (pain lower end of patella), Osgood-Schlatter disease (of TT, restrict activities until pain goes), Sever’s disease (of Achille’s), Scheurmann’s disease (thoracic vertebrae, causes rounded shoulders cos of the pain)
- Osteochondritis dissicans: usually at medial femoral condyle
Describe how DDH is screened for on NIPE
Barlow’s test (can hip be dislocated posteriorly out of acetabulum?) + Ortolani’s (can it be relocated into acetabulum on abduction)
How might you test a child’s motor nerve function after a wrist/elbow #>
Rock - median n (finger flexion)
Paper - radial n (finger extension)
Scissors - ulnar n (finger abduction + adduction)
Okay sign - anterior interosseous branch of median n
