MSK Flashcards

(252 cards)

1
Q

polymyalgia reumatica and risk factors

A

A chronic systemic rheumatic inflammatory disease characterised by aching and morning stiffness in the neck, shoulder and pelvic girdle in people over age 50
PMR is the most common inflammatory rheumatic disease in older people
It is a syndrome associated with synovitis of proximal large joints, tenosynovitis and bursitis
The cause of PMR is unknown although thought to be both genetic and environmental factors contributing to susceptibility and severity

Risk factors:
Older age - highest incidence >65, peak between 70-80
Female (65% cases)
Northern european ancestry - uncommon in middle eastern, asian, african and hispanic descent
Infection - cyclic fluctuations and peak observed in winter and associated with epidemics of mycoplasma, chlamydia pneumoniae and parvovirus B19 infections

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2
Q

polymyalgia reumatica presentation

A

> 50 YO with at least 2 weeks of core symptoms (bilateral shoulder pain, pelvic pain and stiffness lasting >45 mins after rest)

Bilateral shoulder and/or pelvic girdle pain
Initially may be unilateral but quickly becomes bilateral
Worse with movement and interferes with sleep
Shoulder pain may radiate to elbow
Hip and neck pain is main presenting feature in 50-70% cases
Hip pain may radiate to knee
Stiffness lasting at least 48 minutes after waking or periods of rest that may cause them difficulty turning over , rising from bed/chair or raising their arms about their shoulders
Low grade fever, anorexia, weight loss, depression (systemic symptoms in around 50%)
Bilateral upper arm tenderness
Peripheral MSK signs like carpal tunnel syndromes, peripheral arthritis or swelling with pitting oedema of hands, feet, wrists, ankles
Muscles strength not usually impaired but pain may make movement too difficult to assess and can atrophy if prolonged enough without use

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3
Q

polymyalgia reumatica investigations

A

Clinical history and exam
Bloods: ESR; plasma viscosity; CRP usually raised.
Before starting corticosteroids must rule out other conditions with these tests:
FBC, U+Es, LFTs, calcium, alkaline phosphatase, protein electrophoresis, TSH, creatine kinase, rheumatoid factor
Dipstick urinalysis
Urine sample for Bence Jones protein, bloods for Antinuclear Antibody and anti-cyclic citrullinated peptide antibody and CXR
RULE OUT GCA!!

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4
Q

polymyalgia reumatica management, prognosis and complications

A

prednisolone 15mg daily follow up in 1 week to assess if effective
3-4 weeks recheck ESR/plasma viscosity/CRP to assess response and reduce/increase dose accordingly
give patient steroid card and advise on long term steroid complications
refer patients <60, red flags suggesting underlying conditions, no core PMR features or <70% response despite treatment

prognosis:
mostly good response, risk of relapse and long term steroid complications

complications:
GCA occurring spontaneously without warning
steroid complications

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5
Q

fibromyalgia

A

Chronic pain disorder characterised by widespread pain and tenderness
Cause unknown but evidence for genetic predisposition, abnormal stress response system or HP axis and possible triggering events
Thought to be caused by abnormal sensory processing in the CNS making them sensitive to pain and unpleasant sensations
Symptoms are chronic widespread pain associated with unrefreshing sleep and tiredness
Thought that it is more common than reported and underdiagnosed
Usual age of presentation is 20-50 but can be seen in any age
Classification:
Widespread pain involving both sides of body above and below waist as well as axial skeleton for at least three months and presence of 11 tender points among 9 pairs of specified sites (18 points around head, shoulders, elbows, hips and knees)

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6
Q

fibromyalgia risk factors and presentation

A
Risk factors:
Not completing education
Low socioeconomic status
Female
Divorced
Presentation:
Widespread chronic pain: lower back, radiates to buttocks, legs, pain in neck, across shoulders are common
Poor unrefreshing sleep and tiredness
Usually 20-50 YO
Morning stiffness
Paraesthesia
Feeling of joint swelling with no actual swelling
Cognitive problems (memory, difficulty finding words)
Headaches
Light headed/dizziness
Anxiety and depression
Weight fluctuations
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7
Q

fibromyalgia investigations and management

A

Clinical diagnosis

Management:
Conservative: tailored exercise programmes, aquatic therapies, high intensity training, physio
Psychological therapies CBT, relaxation techniques
Acupuncture and massage can be helpful in conjunction
Analgesia: paracetamol, codeine, tramadol
TCA: amitriptyline, nortriptyline
SNRI: venlafaxine, duloxetine, milnacipran
Neuropathic drugs: pregabalin, gabapentin may help reduce pain and sleep problems
Referrals to rheumatology, physiotherapy, mental health, occupational therapy, pain clinic or chronic fatigue service

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8
Q

gout

A

Purine metabolism disorder characterised by raised uric acid in the blood (hyperuricemia) and deposition of monosodium urate crystals in other tissues like soft connective tissues of urinary tract or in joints
Uric acid if end product of purine breakdown and exists as sodium urate at physiological pH
70% urate excretion by kidneys and 30% by GIT

Normal serum uric acid levels are 2.4-6mg/dl (women) and 3.4-7mg/dl (men)

Hyperuricemia usually caused by issue with excretion, overproduction or both
Gout can present without hyperuricemia and vice versa
Gouty arthritis is arthritis due to urate crystals in joints
Gout tends to attack joints in extremities due to lower temperatures enough to precipitate urate from plasma. This tophi typically forms helix of the ear, fingertips, olecranon bursae and other colder sites in body

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9
Q

phases of gout pathology and risk factors

A

Long period of asymptomatic hyperuricemia
Period of acute gout attacks of gouty arthritis followed by arable intervals (months-years) with no symptoms
Chronic tophaceous gout where nodules are affecting joints

Risk factors:
Hyperuricemia: level of urate directly correlates with risk of disease, however gout can occur in people with normal plasma urate levels and many people with high urate never develop gout
Secondary causes of hyperuricemia: HTN, hyperparathyroidism, downs syndrome, lead neuropathy, sarcoidosis, medications, chronic renal disease, volume depletion, glycogen storage diseases, lymphoprliferative/myeloproliferative disorders, carcinomatosis, polycythaemia and severe psoriasis
High purine diet (meat/seafood) alcohol intake
Age
Male
Menopausal status
Obesity, metabolic syndrome, dyslipidemia
Diuretics
Trauma
Family history

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10
Q

presentation of gout

A

Acute pain in joint
Swelling
Erythema
Typically in MTP joints but can occur in knees, midtarsal joints, wrists, ankles, hands and elbows

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11
Q

Gout investigations

A

Joint fluid microscopy and culture - urate crystals or tophi, not usually indicated unless gout in doubt or septic arthritis suspected
The only way to differentiate from pseudogout is crystal analysis!! Gout = negatively birefringent (yellow and needle like). Pseudogout = weakly positively birefringent (blue and rhomboid shaped).

Serum uric acid 4-6 weeks after acute attack to confirm hyperuricemia (crystals form when persistently about 380micromol/L (DOES NOT EXCLUDE GOUT)
Joint XR often normal, nonspecific tissue swelling and cysts may be present
Screen for CVD risk factors and renal disease after diagnosis

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12
Q

Gout management

A

rest, elevate, ice packs, cool environment, avoid trauma
weight loss, avoid seafood, low fat/sugar, high fibre and veg, avoid alcohol, smoking cessation
GOOD = skimmed milk, low fat yogurt, soybeans and cherries. lots of water
vit C supplements

acute medications; NSAIDs (naproxen initially 750mg then 250mg every 8 hrs until attack passes) co-prescribe PPI AVOID aspirin as this INCREASES urate levels!
oral colchicine 500mcg 2-4x daily until symptom relief or nausea/vomiting do NOT exceed 6mg or repeat within 3 days!
short course oral steroids or single IM dose

prophylaxis: lifestyle advice; dietary changes, reducing alcohol and increasing water consumption. Medication is considered if there are >3 attacks/year, a family history or evidence of joint damage

urate lowering therapy first line allopurinol (low dose 50-100mg OD with food increase by 100mg increments every 4 weeks until serum uric acid below 300micromol/L. Max dose 900mg daily divided doses (lower in renal impairment). Risk of precipitating acute attacks
2nd line febuxostat: check LFTs before and after starting. 80mg OD is SUA level >300 after 4 weeks increase dose to 120mg daily aim for SUA <300.
Both of these drugs are xanthine oxidase inhibitors which inhibit xanthine oxidase which prevents conversion of xanthine into uric acid

START URIC ACID THERAPY AFTER ATTACK HAS RESOLVED BUT DO NOT STOP DURING ATTACK IF ALREADY ON DRUGS
Oral colchicine: 500mcg O/TD following allopurinol/febuxostat treatment. Renal impairment doses: eGFR 30-60 500mcg OD; eGFR 10-30 500mcg once every 2-3 days

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13
Q

Gout complications

A

Tophi (firm white nodules under translucent skin) in 50% people with untreated gout after 10 years. Can become inflamed, develop infection, exude tophaceous material
Urinary stones
CKD, MI and CVD
Septic arthritis

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14
Q

osteoarthritis

A

Synovial joint disorder when damage triggers repair process leading to structural changes within the joint
Characterised by bone spurs (osteophytes), loss of cartilage and no major inflammation (mild synovitis)
Commonly due to increasing age but exact cause is unknown; complex multifactorial condition
Joint damage may occur through repeated excessive loading and stress over time or by injury
Any synovial joint can be affected but most commonly in knees, hips and small joints of hands

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15
Q

osteoarthritis risk factors

A
Family history
Increasing age
Female
Obesity
High bone density, low bone density (increased risk of rapid progression of knee and hip)
Joint injury and damage
Joint laxity and reduced muscle strength
Joint malignancy; history of developmental dysplasia; femoroacetabular impingement; leg length discrepancy; varus and valgus knee deformities 
Exercise stresses
Occupational stresses
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16
Q

osteoarthritis presentation

A
Bony swelling and joint deformity
Joint effusions (uncommon except for in knee)
Joint warmth or tenderness (synovitis)
Muscle wasting and weakness
Restricted and painful range of motion, crepitus (grating sound or friction sensation)
Joint instability 
Heberden’s nodes (hands)
other nodes specific to area
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17
Q

osteoarthritis investigations

A

Clinical presentation and history: activity related pain, no morning joint stiffness lasting >30 minutes, functional impairment in those >45 YO
XR for uncertainty, to exclude alternatives or if sudden deterioration: typical features show subchondral bone thickening and cysts; osteophyte formation; loss/narrowing of joint space from cartilage loss
Structural changes may not correlate with functional impairment

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18
Q

osteoarthritis management

A

Weight loss, strengthening exercises and aerobic fitness training. (hands - repetitive grasping, pinching motions etc), appropriate footwear, local heat/cold packs or transcutaneous electrical nerve stimulation (TENS)
ARTHRITIS UK, NHS, ARTHRITIS AND MUSCULOSKELETAL ALLIANCE (ARMA)
Psychological support
Carer assessment and referral PRN
Occupational health assessment
Simple analgesia (paracetamol and topical NSAIDs)
Oral NSAIDs, codeine (30-60mg QDS with paracetamol) or topical capsaicin for moderate-severe pain

Can be given Intra-articular corticosteroid injections to reduce pain and synovitis; not more than 4 injections/year

Hyaluronic acid can be used for intra-articular injection to increase synovial fluid integrity and delay time to surgery

Refer for MDT if symptoms cannot be controlled or have severe impact on quality of life
Eventually may need joint replacement

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19
Q

osteoporosis

A

Disease characterised by low bone mass and structural deterioration of bone tissue with consequent increase in bone fragility and susceptibility to fracture
End result of imbalance of bone remodelling and net turnover by osteoclasts and osteoblasts
During normal ageing, bone breakdown increases and is no longer balanced by osteoblast activity/formation resulting in combination of reduced bone mineral density (BMD) and changes to bone composition, architecture, size and geometry

BMD is the amount of mineral (calcium hydroxyapatite) per unit of bone
Very common in elderly men and postmenopausal women
Pathological fractures are common

Osteoporosis is a BMD of <2.5 standard deviations below mean peak mass (average of young healthy adults) however this does not take into account the bone deterioration so many women without osteoporosis may have fragility fractures

Osteoporosis is considered severe if the patient has experienced one or more fragility fractures

Osteopenia refers to decreased BMD. change can be general or regional. WHO define it as BMD score between -1 and -2.5 standard deviations

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20
Q

postmenopausal osteoporosis

A

After age 30 bone resorption will slightly exceed formation and bone will begin to diminish
In women this can be exacerbated by menopause onset where decline in oestrogen further decrease formation and increase absorption
RANK antigen promotes formation of bone but this is regulated by estrogen and decline results in increased reabsorption
Thickness of cortical and trabecular bone decrease overtime
Vertical fractures are much more common in women
Other factors that affect the rate of decline: lifestyle, medications etc.

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21
Q

risk factors for osteoporosis

A
Old age
Female
white/asian
Small body frame
Genetics 
Hormone imbalances
Low calcium diet, vitamin D or proteins
Sedentary lifestyles/immobility
Diabetes, hyperthyroidism, hyperparathyroidism
GI conditions: crohn's disease, ulcerative colitis, coeliac disease and pancreatitis
CKD, chronic liver disease
BMI <18.5 
Oral steroids (depending on duration and dose)
Smoking
Alcohol >3 units daily
Previous fragility fracture (highest for hip fracture lowest for lower vertebral fracture)
Rheumatological conditions
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22
Q

osteoporosis presentation

A

Asymptomatic and often remains undiagnosed until fragility fracture occurs
An osteoporotic fragility fracture is a fracture occurring as a consequence of osteoporosis.
Fractures often occur at the wrist, spine, hip but can occur at arm, pelvis, ribs and other bones
Fragility fracture is defined as a fracture following a fall from standing height or less although vertebral fractures may occur spontaneously or as result of routine activity like bending or lifting

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23
Q

osteoporosis investigations

A

DEXA scan for BMD: osteoporosis is a BMD of <2.5 standard deviations below mean peak mass (average of young healthy adults)
T score to calculate fragility fracture risk: QFracture score: >10% high risk; close to but <10% intermediate and low risk is <10% (FRAX score red high risk, orange mod and green low risk)
Clinical history or diet; Identify risk factors for falls: imapaired vision, neuromuscular weakness/incoordination, cognitive impairment, use of alcohol and sedative drugs
Bloods: vitamin D deficiency

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24
Q

osteoporosis management and complications

A

All patients should be encouraged to increase dietary intake of Ca and vitamin D

Bisphosphonates for high/intermediate risk of fragility fractures. Alendronate 10mg OD or 70mf once weekly or risedronate 5mg OD or 35mg once weekly if not CI. MUST TAKE AT LEAST 30MINS BEFORE BREAKFAST ON EMPTY STOMACH. TAKE RISEDRONATE AT LEAST 2 HOURS EITHER SIDE OF FOOD. MUST SWALLOW WHOLE WITH AT LEAST 200ML WATER. DO NOT SUCK OR CHEW (oropharyngeal ulceration). SIT UPRIGHT AND DONT LIE DOWN FOR 30 MINS. DO NOT TAKE AT BEDTIME/BEFORE GETTING UP. TAKE WEEKLY PREP SAME TIME EACH WEEK. MINIMUM OF 30 MINS BETWEEN TAKING CALCIUM SUPPLEMENT OR ANTACID (changes absorption)
side effects include nausea, vomiting, mild gastritis, abdo pain in first month, bone, joint or muscle pain, oesophagitis

Assess for vitamin D deficiency and inadequate calcium intake and prescribe cholecalciferol (Calcichew D3 forte tablets) 1250mg Ca carbonate (500mg Ca) and 400 units of vitamin D3 for supplementation if needed

Identify risk factors for falls: impaired vision, neuromuscular weakness/incoordination, cognitive impairment, use of alcohol and sedative drugs

For those who do not qualify for medication, give lifestyle advice and review in 5 years time

Complications:
Hip fracture
Vertebral fracture
Severe kyphosis causing breathing difficulty 
Reduced quality of life
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25
limping (children)
Defined as an asymmetric gait that is a deviation from the normal goat pattern expected for a child’s age Causes can vary from benign to potentially life threatening (infection, tumours, child abuse - non-accidental injury NAI - etc) Appropriate evaluation is needed to assess potential causes and red flags Assessment depends on if the limp is acute or chronic Trauma is the most common cause of limping Persistence of primitive reflexes beyond 6 months is suggestive of neurological problems such as cerebral palsy
26
normal gait pattern in children and atypical gaits
Broad based gait for support, appears to be high stepped and flat footed Arms outstretched for balance Legs extremely rotated with degree of bowing Heel strike develops at around 15-18 months with reciprocal arm swing Running and change of direction occur after age 2 School age children increase step length and frequency slows. Adult gait and posture occur around age 8 Normal gait has considerable variations and the ages they appear and change at can appear to be family related
27
normal variation in children's gait
``` concern can arise if these persist beyond normal age range, are progressive or asymmetric, if there is pain or functional limitation can be evidence of neuro disease If the child is short (less than 25th centile) and has bow legs or knock knees consider XRs for suspicion of hypophosphatemic rickets or skeletal dysplasias Alignment varies with age and often influenced by family history of same pattern Habitual toe walking is common up to 3 years. Persistence of this can be due to persistent femoral anteversion and is characterised by child walking with patella and feet pointing inwards (between ages 3-8) Internal tibial torsion is characterised by walking with patella facing forwards and toes pointing inwards (common up until 3 YO) Metatarsus adductus is characterised by a flexible C shaped lateral border of foot. Most resolve by age 6 Bow legs (genu varum) are common from birth to early toddler often with out-toeing (maximal at approx. 1 YO) most resolve by 18 months Flat feet. Most children have flexible feet with normal arch on tiptoeing. Flat feet usually resolve by age of 6 ```
28
normal motor milestones in children
sit without support - 6-8 months creep on hands and knees 9-11 months cruise or bum shuffle 11-12 months walk independently 12-14 months climb up stairs on hands and knees 15 months run stiffly 16 months walk down steps (non-reciprocal) 20-24 months walk up steps alternate feet 3 years hop on one foot, broad jump 4 years skipping 5 years balance on one foot for 20 seconds 6-7 years
29
abnormal gait patterns and indications in children
Antalgic gait: reduced time spent on weight bearing on affected side. Possible causes include trauma and spinal osteomyelitis. Presents with unwillingness to bear weight on foot. May also be seen in juvenile idiopathic arthritis although not always painful Circumduction (peg leg): excessive hip abduction as leg swings forward. Typically seen with leg length discrepancy, stiff/restricted movement in joint or unilateral spasticity in hemiplegic cerebral palsy Spastic gait: stiff, foot dragging with foot inversion. Often seen in UMN disease (diplegic or quadriplegic cerebral palsy or stroke) Ataxic gait: instability with alternating narrow to wide base. Seen in ataxic cerebral palsy affecting cerebellum, cerebellar ataxia and friedreich’s ataxia Trendelenburg’s gait: results from hip abductor weakness. Weight bearing on the ipsilateral side, pelvis drops on the contralateral side rather than rising normally. Waddling sailors gait with hips, knees and feet externally rotated. Legg-Calve-Perthes disease, slipped capital femoral epiphysis, developmental dysplasia of hip, inherited myopathies etc. Toe walking “equinus”: habitual toe walking is common in children and associates with normal tone, range of movement and walking. Persistent toe walking is seen in spastic UMN disease (diplegic cerebral palsy) and can be presentation of mild lysosomal storage disorder Stepping: entire leg lifted at the hip to assist ground clearance. Occurs with weak ankle dorsiflexion, compensated by increased knee flexion (foot drop gait). LMN disease eg spina bifida or polio and peripheral neuropathies like Charcot-Marie-Tooth disease Clumsy gait: commonly used to describe difficulty with motor coordination (fine and gross). May have frequent falls, difficulty with self help skills like dressing or feeding. Poor handwriting and learning disabilities. Important to exclude neurological disability (cerebral palsy, cerebellar ataxia or LMN disorders) as well as inflammatory arthritis, myopathies, orthopaedic problems and metabolic disorders
30
limping history taking
History taking: always check medical records of previous hospital visits for possibility of child maltreatment Duration and progression of limp Acute onset - trauma, infection or inflammation Any precipitating trauma? Viral infection? (transient synovitis or reactive arthritis) Any associated pain? Nature of pain, location, severity, timing of pain (worse moving or at rest?) Constant localising pain may indicate fracture, osteomyelitis or septic arthritis Infants: pain during nappy changing indicates discitis Associated muscle weakness? Neuromuscular disease Birth and developmental history including walking onset, neurodevelopmental delay or regression, risk factors for developmental dysplasia of hip PRN Delay in motor milestones suggests neuromuscular cause, while regression suggests acquired disease (inflammatory arthritis) Family history of rheumatological or neuromuscular disease (juvenile idiopathic arthritis; Muscular dystrophy)
31
general and pGAL examination
CHECK FOR: Pyrexia and tachycardia - sepsis Pallor, irritability or lethargy - sepsis/systemic disease Unexplained rash or bruising - haematological or inflammatory joint disease or child mistreatment Generalised LAP or rash - infection, inflammatory joint or haematological disease Height and weight of child and compare to prior visits - poor growth may indicate underlying chronic disease pGAL (paediatric gait, arms, legs and spine) assessment: Look Check that the child can weight bear. Check for scoliosis, tufts of hair on the spine or a sacral pit — may indicate spina bifida. Check for leg length discrepancy or pelvis asymmetry. Compare both lower limbs looking for joint asymmetry, erythema, swelling, bruising, lacerations, or deformity. Check for calf muscle hypertrophy — may indicate muscular dystrophy. Check for signs of evolving compartment syndrome, including agitation, pain disproportionate to the injury, and palpable swelling. Feel Check for focal bony and muscle tenderness, swelling, or heat over the spine, pelvis, lower limbs, abdomen, and testicles (if appropriate). Check for pulses and carry out a peripheral neurological examination of the lower limbs to assess for neurovascular compromise. Move Depending on the child's age, examine the gait (including walking on heels and tiptoes and running) looking for a gait abnormality, such as an antalgic or Trendelenburg gait. Assess the range of movement in each joint, especially the hip. Children presenting with knee pain may have referred pain from the hip. Examine the joints adjacent to the affected joint to rule out referred pain
32
red flags of limping gait
Pain causing waking at night - malignancy Redness, swelling or stiffness of joint/limb - infection or inflammatory joint disease Weight loss, anorexia, fever, night sweats, fatigue - malignancy, infection or inflammation Unexplained rash or bruising - haematological or inflammatory joint disease or child maltreatment Limp and stiffness worse in morning - inflammatory joint disease Unable to weight bear or painful limitation of range of motion - trauma or infection Severe pain, anxiety, agitation after traumatic injury - neurovascular compromise or impending compartment syndrome Palpable mass - malignancy or infection
33
management of limp in children
Safeguard for abuse concerns Suspected neurological condition: refer to neurology for further testing/investigate underlying condition ACR appropriateness criteria: guidelines for referrals and best imaging/treatments for specific conditions Any history of trauma or focal bony tenderness on examination, XR indicated If the child is aged 3–9 years, well, afebrile, mobile but limping, and has had the symptoms for less than 72 hours (or more than 72 hours and improving): Consider a working diagnosis of transient synovitis. Symptom relief with rest and simple analgesia, paracetamol and ibuprofen. safety net Follow up in 48–72 hours and again in 1 week to reassess. If a working diagnosis of a sprain or strain is made: Analgesia for symptoms relief, rest PRICE (protection, rest, ice, compression, elevation) Advise on safe return to usual activity and risks for re-injury Follow up medical review 5-7 days after Arrange referral to physio if not improving on ongoing symptoms Arrange orthopedic referral if recovery slower than expected, worsening or new symptoms or symptoms are out of proportion to injury If there is a history of trauma or focal bony tenderness on examination and there are no indications for referral: Arrange for a same day X-ray. If the child has persistent limp with a normal initial X-ray, refer to paediatric orthopaedics or rheumatology (the urgency depending on clinical judgement) for further investigation.
34
urgent/non-urgent referrals for children limping gait
Urgent Referral: Fever and/or red flag suggesting serious pathology Suspected of mistreatment Younger than 3 YO - transient synovitis is rare in this age group; septic arthritis is more common Older than 9 YO with painful restricted hip movements (internal rotation in particular) to exclude upper femoral epiphysis Referral (yellow flags): Cause cannot be managed in primary care Uncertainty of cause Presents with limp on multiple occasions Persistent limp and normal XR refer to paediatric orthopaedics/rheumatology
35
strains
Strains are the stretch/tear of muscle fibres or tendons Tissue stretched beyond its limit or forced to contract too strongly Typically affect the hamstring, foot or back Classified by: First degree mild strain: few fibres stretched or torn, area is painful and tender, retains normal strength, power may be limited by pain Second degree moderate strain: several fibres injured, more severe pain and tenderness, mild swelling, noticeable loss of strength, sometimes visible bruising Third degree severe strain: tissues tear all the way through, may sometimes produce popping sensation, total loss of function, severe pain and swelling, visible bruise, difficult weight bearing. Can cause lifelong weakness if severe or doesn’t heal well
36
sprains
Stretch or tear of a ligament Occurs as result of abnormal or excessive forces applied to joint Typically affects the ankles, knees, wrists and thumbs Classification: Grade I: mild stretching of ligament, joints are stable Grade II: partial rupture of ligament but joint remains stable Grade III: complete rupture of ligament, joint instability
37
general sprain/strain presentation and investigations
``` General symptoms: Pain, tenderness or weakness of the area Swelling or bruising Inability to bear weight Muscle spasms or cramping where muscles painfully tighten on their own ``` Diagnosis: Clinical diagnosis Imaging (XR/MRI/CT check for tissue damages)
38
strain/sprain general management and complications
Pay the PRICE and avoid HARM (for 72 hours) PRICE: PROTECT from further injury REST - stop exercise or activity for 48-72 hours, try not to put weight on injury ICE - apply ice packs for up to 20 minutes every 2-3 hours, first 48-72 hours after injury COMPRESSION - simple elastic bandage or tubular bandage, snug not tight, controls swelling ELEVATE injured area especially lower limbs Try not to leave immobile for prolonged time; short period of immobilization may be needed for few days in severe injury; advise on safe return to usual activities by starting with active mobilisation and flexibility range of motion exercises as soon as tolerable without excessive pain Simple analgesia Most improve after 2 weeks; avoid strenuous exercise for up to 8 weeks, can take months for severe injury Arrange medical review or follow up after 5-7 days to check healing, worsening symptoms etc. Refer to physiotherapy if ongoing >8 weeks, if no improvement for long time consider surgery referral to avoid long term complications Avoid HARM for 72 hours: Heat: encourages bruising and inflammation Alcohol: increases bleeding and swelling and decreases healing Running or any other activity affecting the whole body: may cause further damage Massage: may increase bleed or swelling Complications: Loss of joint movement Joint instability Osteoarthritis
39
acromioclavicular joint disruption
Most mobile joint in the body High mobility increases risk of injury Shoulder pain is the third most common cause of MSK consultations in primary care Loose joint capsule relies on rotator cuff muscles and tendons to keep it stable Shoulder strains: muscles and tendons are overstretched or torn, common Shoulder sprains: ligaments damaged by stretching or impact The acromioclavicular ligament is most frequently injured: called shoulder separation mild/moderate - small or partial tear, mild pain, some swelling, reduce, painful shoulder movement Severe - ligament torn, joint separates and dislocates coracoclavicular ligament can also be injured in more severe injuries
40
rockwood classification of acromioclavicular joint disruption
type I - AC ligament sprain, CC intact and clavicle non-displaced type II - complete disruption of AC, sprained CC and up to 25% superior displacement of clavicle type III - completed disruption of AC and CC, 25-50% superior displacement of clavicle type IV - complete disruption of AC and CC, posterior displacement of clavicle through trapezius type V - complete disruption of AC and CC and extreme upward displacement of clavicle type VI - complete disruption of AC and CC with inferior displacement of clavicle
41
presentation and management of acromioclavicular joint disruption
Mild: sudden pain, weakness, limited range of motion, swelling and bruising with examination showing painful movement and swelling Severe AC joint disruption: marked tenderness, visible or palpable step if clavicle has separated Management: Examine for injury to vessels or nerves Mild AC disruption: broad arm sling for 2-3 weeks, simple analgesia, encourage to keep shoulder moving to avoid adhesive capsulitis Severe: XR or USS, identify damaged structures, classify injury, types 3-6 need orthopaedic treatment - refer
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wrist sprains
Ligaments of wrists are stretched or torn often from falling onto outstretched hand Ligaments of the hand: radiocarpal, ulnar carpal, transverse metacarpals dorsal and palmar, interphalangeal ligaments also dorsal and palmar 3 grades: Grade I ligaments stretched or torn slightly Grade II partially torn - may cause some loss of function Grade III completely torn - requires surgical input, possibility of avulsion fracture (small chip of bone taken off with ligament)
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finger sprains
Most commonly the PIP joints Volar or palmar or plate ligaments Longitudinal force applied eg ball hitting end of the finger forces hyperextension of ligament Metacarpophalangeal joint in the thumb most commonly affected called ‘skier’s thumb’ where ulnar collateral ligament is sprained. Repetitive injury to this ligament is called ‘gamekeeper's thumb’
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management of wrist/finger Sprains
``` History and examination XR if avulsion fracture suspected mild/moderate: PRICE to support injured tissues Severe - surgical referral Simple analgesia Physiotherapy ```
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mallet finger and management
Injury to extensor tendon at distal phalanx Role of tendon is to keep digit straight Rupture flexion deformity Caused by object striking tip of finger forcing bending further than normal and rupturing the tendon Management: Exam: usually painful, swollen and bruised, noticeable droop XR to rule out intraarticular fracture Treat in splint for 8 weeks: hold finger in straight position must be worn at all times After 8 weeks can be removed gradually for increasing periods of time Failure to heal after 8 weeks or large avulsion or subluxation of joint needs surgical referral for pinning to hold in place
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back sprain and strain and presentation
Causes mechanical back pain Lumbar region bears most weight when moving, twisting and bending so is most common Exact nature of injury difficult to ascertain: soft tissues become inflamed, muscles may spasm causing pain, aching, burning, stabbing, sharp or dull, reduced movement, may last for weeks or become chronic ``` presentation: tenderness in the lower back Pain that occurs suddenly Muscle spasm Pain on when standing, walking, or twisting Stiffness Pain that radiates to the legs, buttock, or thighs Weakness in muscles and tendons ```
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management of back sprain or strain
``` Clinical history and exam Continue activity - bed rest worsens outcome Simple analgesia Review after 2-6 weeks Consider physiotherapy referral ``` ``` exclude: cauda equina fracture cancer infection ```
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whiplash
Term used to describe injury to the neck occuring after sudden movement of neck, vigorous movement damages ligaments and tendons in the neck Most common after vehicle accidents Classification: Grade I: neck pain and associated symptoms, absence of objective physical signs Grade II: neck pain, associated symptoms, objective physical signs, no evidence of neurological involvement Grade III: neck pain, associated symptoms, evidence of neurological involvement including decreased or absent reflexes, decrease or limited sensation or muscular weakness IV: neck pain, associated symptoms with evidence of fracture of dislocation
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whiplash presentation
May not experience symptoms immediately after injury Start to feel pain, stiffness and temporary loss of movement in neck over the following 6-48 hours Symptoms peak at about 2 days Gradually improve may last few weeks Headaches Muscle spasms Pain in shoulders
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whiplash investigations and red flags
Full spine and neurological examination Do not examine neck until risk of fracture or serious injury are ruled out Features of serious head/neck injury: altered consciousness, FND or paraesthesia in extremities, midline cervical tenderness Risk factors for serious injury: immediate onset neck pain after event, >65 YO, drowning or diving accident, multiple fractures, significant head or facial injury, dangerous mechanism of injury (fall greater than 1 m) or side impact collision, rigid spinal disease (ankylosing spondylitis), unable to walk about or sit following injury
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management of whiplash
Reassurance of recovery within 2-3 months, encourage early return to usual activities and early mobilisation Explain maintenance of normal activity are important for recovery and restriction of this might delay recovery Oral analgesia Physiotherapy referral Psychology referral if patient has poor expectation or thought of ongoing disability, symptoms of acute stress disorders (within 4 weeks of injury), PTSD, anxiety or depression Follow up at 7 days, 6 weeks and 3 months unless condition resolves
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knee MCL injury
Most common ISOLATED ligamentous knee injury Runs between medial epicondyle of femur and anteriomedial aspect of tibia with deep attachment to medial meniscus Prevents lateral movement of tibia Mechanisms of injury often direct impact to lateral aspect of knee or twisting injury Valgus stress test to determine rupture Valgus (outward angulation) stress test: Pt lying flat legs extended relaxed Hold leg above ankle with one hand and other on lateral thigh Externally rotate thigh slightly Passively adduct femur (apply pressure on lateral thigh) Repeat test at 20-30 degree knee flexion Look for excessive gapping on medial knee joint and pain
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knee LCL injury
Runs between lateral epicondyle of femur and head of fibula Prevents medial movement of tibia on femur Stress placed on medial side of knee or twisting injury mechanisms of injury Varus stress test diagnosis Less common than MCL injury and often more debilitating Varus (inward angulation) stress test: Pt lying supine relaxed legs Hold lower leg above ankle and medial side femur with other Laterally rotate leg Apply pressure to medial thigh (passively abducting) Repeat test with knee in 20-30 degrees flexion Look for excessive gapping on lateral side of knee joint and pain
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management of collateral ligament injury in knee
History and exam MRI to delineate degree of ligament disruption PRICE protocol: non-weight bearing sufficient for mild injury Knee splint Quads strengthening exercises are essential for knee stability Orthopaedic input for grade III injuries as unlikely to heal without surgical input
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ACL knee injury
Runs between front of tibial plateau and posterolateral aspect of intercondylar notch of femur Controls rotational movement Prevents forward movement of tibia in relation to femur Injuries occur frequently as result of pivoting mechanisms - flexed knee suffers sudden twist with foot firmly on ground (football, basketball, skiers) Severe sudden pain, audible pop, patient unable to bear weight due to hemarthrosis formation (blood collection) Anterior draw test to diagnose XR likely normal, MRI to confirm ACL disruption Arthroscopy to assess integrity and repair if needed Anterior draw test: First exclude PCL injury to avoid a false positive result Pt lying flat Flex hip and knee 90 degrees rest foot on bed Palpate joint line with thumbs aside patella and palms around back of joint Use explosive force to move tibia anteriorly +ve test if tibia moves anterior >6mm or feel soft mushy end feel Other tests for ACL tear: pivot shift or lackman test
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PCL knee injury
Runs between posterior tibial plateau and medial aspect of intercondylar notch of femur Prevents forward sliding of femur in relation to tibial plateau Vital for support when walking down hills or stairs Injury caused by hyperflexion eg falling onto bent knee or proximal tibia hits dashboard (car injury) Immediate pain and swelling, can usually weight bear following event Posterior drawer tests to assess PCL integrity Posterior sag of tibia seen in exam XR may show avulsion fractures MRI shows rupture Isolated PCL injury: non-surgical treatment, pain management, non-weight bearing immobilisation and physiotherapy Surgery indicated for other injuries to knee, avulsion fractures, or if conservative management fails Posterior draw test: Pt lying supine, flex hip and knee to 90 degrees Grasp knee with both hands thumbs upward either side of patella and palms around joint Apply fast hard force in posterior direction +ve test if tibia moves posterior >6mm or feels soft and mushy feeling Look for posterior sag sign (tibia naturally sags back further than normal in flexed knee supine position)
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Osgood-Schlatter disease
Common cause of knee pain in adolescents Related to tendons: repeated pulling on tendons on the growth plate of the tibia causing repeated microtrauma, inflammation of apophysis resulting in apophysitis Experience pain in knee over tibial tuberosity during activity like running or jumping Usually unilateral but can be bilateral (30%) More common in boys during periods of rapid growth Localised pain worse with activity and improves with rest
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Osgood-Schlatter disease investigation and management
Examination shows swollen, tender tibial tuberosity Range of movement not affected No effusion present Exam hip for referred knee pain XR not usually recommended as often normal Management: Settles over weeks or months but can persist for 1-2 years Simple analgesia Intermittent ice pack application especially after activity Patients may continue normal activity but may need to modify duration, frequency or intensity (limit running and jumping)
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plantar fasciitis and presentation
Tought, long thin ligament (plantar fascia) lies beneath skin on sole of foot, connects the heel to front of the foot, provides support to arch and absorbs stress placed on foot Excessive pressure causes microtears resulting in stiffness and pain Occurs often without identified cause: insidious onset, new, repetitive activity can cause, obesity, high arch, excessive flat foot or tight calf muscles can contribute to injury Presentation: Pain near heel Present on first few steps after rising, subsides after walking, will benign to worsen again with increasing time on the feet
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investigations and management for plantar fasciitis
Exam shows tender on palpation Associated with tightness of achilles tendon Limited dorsiflexion Management: Weight loss, cushioned shoes, avoid barefoot walking, foot rest Stretching exercises, simple analgesia Icepacks No improvement: podiatry/physiotherapy referral Orthopaedic referral/advice Steroid injections under USS guidance
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achilles tendon rupture and presentation
Thickest tendon in human body attached to calf muscle to heel (calcaneus) Rupture common between 30-50 YO in activities requiring forceful push off with feet Risk factors include: increasing age, history of tendinopathy, steroid excess, quinolone antibiotics Presentation: Sudden snap or sensation of being hit in back of ankle Acute sharp pain Unable to stand on tiptoe Localised swelling Palpable defect of tendon if complete rupture Active planetary flexion will be weak Absence of normal plantar flexion on squeezing calf muscle indicates complete tension rupture (thompson test)
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achilles tendon rupture investigation and management
Thompson test: prone lying position feet hanging off the bed. Squeeze calf few times to observe plantar flexion/absence indicates rupture USS/MRI unclear diagnosis Management: Orthopaedic referral Advise not to weight bear Analgesia Surgical management to reduce risk of re-rupture, recommended for those with high activity Conservative management in older/less active people using sequential casting
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ankle sprain
Lateral sprain most common (85%) Inversion and plantar flexion injuries can lead to damage to anterior talofibular or calcaneofibular ligaments Medial ligament sprains are more likely to happen in conjunction with lateral malleolar or fibular fractures and have much more complex injury pattern Grading: Grade I: stretched ligament, microscopic tearing, mild swelling, little/no functional loss, no joint instability, bears weight at least partially Grade II: stretched, parietal tearing, moderate swelling, bruising (ecchymosis), moderate functional loss, mild/mod joint instability, difficulty weight bearing Grade III: completely ruptured, swelling immediately and severe, ecchymosis, patient cannot bear weight, mod-severe instability of joint
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management of ankle sprains/strains
Grade I/II: PRICE, NSAIDs, most heal well with range of motion exercises Grade III: short immobilisation period, below knee cast or brace, physiotherapy, vaoid vigorous exercise for at least 3-4 weeks Surgical repair is fully torn or joint is unstable
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history taking for sprain or strain and possible indications
Mechanism of injury: sudden rapid inversion/internal rotation of ankle suggests lateral ankle sprain Acute hamstring strains present typically suddenly after sprinting Risk factors for physical abuse or domestic violence - other bruising, previous hospital visits, stories not adding up to injury etc. Symptom severity and duration: sprain typically includes pain around the affected joint, tenderness, swelling, bruising, pain on weight-bearing, and decreased function. Symptoms of a strain typically include muscle pain, cramping, and spasm; muscle weakness, inflammation, and/or bruising. A 'pop' heard or felt at the time of injury may suggest an anterior cruciate ligament knee injury or hamstring strain. Features of chronic joint instability include persistent pain, swelling, perception of the joint 'giving way' with weight-bearing, recurrent injury, and persistent reduced function (particularly if a sprain is severe or in recurrent injury). Note: the severity of symptoms depends on the severity of the injury as well as time since injury. Symptom duration of more than a few days can suggest more severe injury. The person's usual physical activity level. Any other risk factors for injury or re-injury. Any previous sprain, strain, or joint instability, including treatments and outcome. Use of any current bracing or taping.
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examination of sprain/strain
Examine the person for typical signs and possible complications. Observe for signs of swelling, bruising, limb deformity, or asymmetry/misalignment that may suggest fracture or dislocation. Note: it can take up to 24 hours for the full extent of bruising to become apparent. Note: examination of an acutely injured or painful joint can be difficult owing to pain, swelling, and guarding. Palpate the joint or muscle, including for point tenderness and joint line tenderness. Replication of the person’s ‘known pain’ on palpation and/or stressing of a ligament may indicate ligament injury. Assess the range of joint movement, strength testing, signs of joint instability, coordination and balance, ability to weight-bear, and gait. Perform additional specific joint tests, such as the anterior drawer test of the ankle, if clinically appropriate. In ankle injuries with bruising and pain on palpation around the distal fibula, and/or a positive anterior drawer test, a rupture of the lateral ankle ligaments is likely. In hamstring injuries, examination of the hip and lumbar spine should also be performed to identify any other potential causes of posterior thigh pain. Perform a neurovascular examination to assess for peripheral nerve injury and check peripheral pulses are intact and symmetrical.
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X ray criteria for sprain and strains
Ottawa rules recommend an XR in the following cases: - Following an ankle injury, if there is pain in the malleolar zone, and one of the following: Inability to bear weight (walk four steps) immediately after the injury and when examined. - Bone tenderness along the distal 6 cm of the posterior edge of the fibula or tip of the lateral malleolus. - Bone tenderness along the distal 6 cm of the posterior edge of the tibia or tip of the medial malleolus. Following a foot injury, if there is pain in the midfoot zone, and one of the following: - Inability to bear weight (walk four steps) immediately after the injury and when examined. - Bone tenderness at the base of the fifth metatarsal. - Bone tenderness of the navicular bone. Following a knee injury, if there is one or more of the following: Inability to bear weight (walk four steps) at the time of injury and when examined. - The person is aged 55 years or more. - Tenderness at the head of the fibula. - Isolated tenderness of the patella. - Inability to flex the knee to 90 degrees. An X-ray is also recommended: Following a wrist injury, if there is: - Pain or tenderness over the scaphoid bone (palpate at the base of the anatomical snuff box and scaphoid tubercle). Note: the Ottawa rules may be less applicable in certain clinical situations where clinical judgement should be used, for example in people who: Are younger than 18 years of age. - Are confused, have a cognitive deficit, communication problems, or are intoxicated, as the person's expression or perception of pain can be altered. - Have polytrauma, head injury, or diminished sensation in the lower extremities (for example due to neurological deficit). - Have gross swelling making palpation of the area impossible. - Are pregnant.
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osteomyelitis
Refers to infection of the bone marrow which may spread to the bone cortex and periosteum via the Haversian canals Due to bone being naturally ischaemic tissue it is more vulnerable to infections Results in inflammatory destruction of bone and if periosteum is involved, necrosis When necrotic bone becomes detached from healthy bone it is known as a sequestrum A large sequestrum that remains in situ acts as a focus for ongoing infection Involucrum refers to a viable periosteum that has separated from the underlying bone which forms new bone around it. In acute and chronic disease there is subsequent bone remodelling and often associated deformity Most common site of infection is the distal femur and proximal tibia in children and cancellous bone in adults Incidence of chronic osteomyelitis is increases due to prevalence of predisposing conditions like diabetes and PAD increasing Acute, haematogenous type occurs more in children while chronic direct contagious type occurs more in adults Osteomyelitis may be acute or chronic and can be categorised into two main subgroups: haematogenous and direct osteomyelitis
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osteomyelitis pathology
Leads to cortex erosion with holes (cloacae) Exudation of pus lifts up periosteum, interrupting blood supply to underlying bone and necrotic fragments of bone may form (sequestrum = infected dead bone) Presence of sequestra is typical of chronic infection New bone formation created by elevated periosteum forming an involucrum Pus may discharge into joint spaces septic arthritis or via sinuses to the skin
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haematogenous osteomyelitis vs direct (contiguous) osteomyelitis
Haematogenous osteomyelitis: Infection resulting from haematological bacterial seeding from remote source More commonly associated with children where it tends to occur in rapidly growing and highly vascular metaphysis of growing bones Haematogenous osteomyelitis also seen in patients with distance foci of infection, such as those with urinary catheters Occurs more commonly in children Direct (contiguous) osteomyelitis: Type of infection where there is direct contact of infected tissue with bone; may occur during surgical procedure or following trauma Clinical signs tend to be more localised and often has multiple organs involved Occurs more often in adults
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acute vs chronic osteomyelitis
Acute: Haematogenous spread from abscesses, pneumonia, genitourinary instrumentation Local infection spread from boils or abscesses Chronic: All types of acute osteomyelitis can end in chronic Considered a complication of acute condition
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pathogens commonly causing osteomyelitis and risk factors
``` Pathogens: Staph Aureus is most common including MRSA strains H. influenzae Strep. E. coli Proteus Pseudomonas Salmonella ``` ``` Risk factors: Trauma/surgery Prosthetic orthopaedic device Vascular disease Diabetes PAD Chronic joint disease Alcoholism IV drug abuse Chronic steroid use Immunosuppression TB HIV/AIDs Sickle cell disease Presence of catheter related bloodstream infection Open fractures ```
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osteomyelitis pattern of infection
Adults - Cancellous bone - Vertebrae (IV drug users) and Feet (diabetics) Children - Metaphysis of long bone (more vascular) - Distal femur or upper tibia
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complications and prognosis of osteomyelitis
Septic arthritis Fractures Deformity Chronic osteomyelitis ``` Bone abscess Bacteraemia Fracture Growth arrest Septic arthritis Cellulitis Chronic infection ``` Prognosis: Variable depending on risk factors and general condition Timely diagnosis and intervention in otherwise well patient should lead to full recovery although need monitoring for relapse over several months
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general presentation osteomyelitis
gradual onset pain over few days tenderness, warmth and erythema at affected part unwilling to move affected limb slight effusion in neighbouring joints signs of systemic infection (fever, tachycardia, tachypnea, anorexia)
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haematogenous osteomyelitis presentation
Long bone Acutely febrile and bacteraemic Markedly painful immobile limb May be swelling and extreme tenderness with erythema and skin is warm around affected area Pain exacerbated by movement and may be sympathetic effusion of neighbouring joints In neonates and infants may be associated septic arthritis Occasionally may present with mild symptoms, history of blunt trauma 24-48 hours previously with mild or no pyrexia May be nonspecific malaise and suspicion only raised as symptoms begin to localise over several days Vertebral: Usually insidious presentation following acute septicaemic episode May have localised oedema, erythema and tenderness with/without associated contagious vascular insufficiency Alternatively can have chronic back pain worse at rest with unremitting nature May have night pains which can be associated with nonspecific malaise Pott's disease: Vertebral osteomyelitis resulting from haematogenous spread of TB Damage to bodies of two neighbouring vertebrae leading to vertebral collapse and subsequent abscess formation (cold abscess) Pus can track out from there into adjacent structures leading to systemic symptoms of malaise, fever and night sweats
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contiguous osteomyelitis presentation
Patients tend to present in classic manner with fever, pain and erythema Acutely febrile and bacteraemic Markedly painful immobile limb May be swelling and extreme tenderness with erythema and skin is warm around affected area Pain exacerbated by movement and may be sympathetic effusion of neighbouring joints In neonates and infants may be associated septic arthritis May have associated history os accidental or surgical trauma
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chronic osteomyelitis presentation
Previous acute infection (either unresponsive to treatment or relapsing) Localised bone pain Erythema and swelling over affected area Non healing ulcer Draining sinus tracts Decreased range of motion of adjacent joints Chronic fatigue Generalised malaise **Diabetic foot ulcers may also be present and pain may be masked by neuropathy!!
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osteomyelitis investigations
Bloods: FBC; ESR; CRP Blood cultures and mandatory and +ve in 60% cases Pus/swab cultures Bone biopsy and cultures GOLD STANDARD but rarely needed for acute Chronic osteomyelitis is more difficult to diagnose as blood cultures often come back normal MRI - acute Isotope bone scans for prosthesis XR - chronic changes after 10-14 days, haziness, loss of density, subperiosteal reaction, sequestrum and involucrum *IF MYCOBACTERIAL OR FUNGAL INFECTION IS SUSPECTED MUST INFORM MICRO as need different growth medium*
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management of osteomyelitis
Success is closely linked to surgical debridement and adequate antibiotic therapy Extensive surgical cleaning with antibiotic therapy for 4-6 weeks (flucloxacillin +/- fusidic acid FIRST LINE, clindamycin for allergy or vancomycin if MRSA suspected) Pseudomonas osteomyelitis give ciprofloxacin 500mg/8-12 hr PO Chronic infections need extensive surgical debridement, removal of implants and antibiotic therapy lasting 3-6 months Chronic infection is often beneficial to delay treatment until culture and sensitivity results are obtained. Analgesia for symptom control Seek specialist advice is chronic infection or prosthesis are involved Local treatments: Local bone and soft tissue debridement Stabilise bone Local antibiotic therapy Reconstruct soft tissue and osseous defect zone
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potts disease
Caused only in spinal TB (aka tuberculosis spondylitis) Infection in the anterior vertebral body (more oxygenated blood) leads to degeneration and compression fracture of vertebrae causing wedging deformity (Hump kyphosis) More common presentation is cold abscess formation. Painless, slow growing fluctuation swelling. Presents in cervical Pott: mediastinal mass; thoracic Pott: iliac fossa mass/swelling; lumbar Pott: groin/femoral below inguinal ligament mass/swelling
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septic arthritis
Infection of 1 or more joints (native or prosthetic) caused by pathogenic inoculation of microbes, usually pyogenic bacteria (fungi and virus’ are rare) Occurs either by direct inoculation or via haematogenous spread Incidence increases 10 fold in patients with underlying joint disease or with prosthetic joints Can be acute or chronic and is a medical emergency - delay in treatment can result in septicaemia, septic shock and irreversible joint destruction (osteoarthritis) leading to long term disability Can destroy a joint in under 24 hours and mortality is up to 11% Must treat all acute swelling and painful joints with systemic symptoms as septic arthritis until proven otherwise Knee joint is most often affected Pathology: Acute inflammation with effusion (if treated earlier can have full resolution) Suppuration with tissue destruction (often causes septicaemia) Healing with osteoarthritis of the joint
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common causes of septic arthritis and route of infection
``` Staph aureus Streptococci Gonococcus Gram -ve bacteria Meningococcus TB ``` Route of infection: Direct injury: trauma, surgery, arthroscopy, intra-articular injection Haematogenic: infected skin lesion, other infection sites Immunodeficiency and prosthesis facilitates spread of infection
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risk factors for septic arthritis
Underlying joint disease (osteoarthritis, RA) Prosthetic joints (increases tenfold) >80 YO IV drug users/chronic IV treatments/indwelling lines Immunocompromised (HIV/diabetes/alcohol misuse/medications) Contiguous spread: cutaneous ulcers or skin infection. Can lead to bacteraemia and subsequent seeding of infection in a joint Areas where lyme disease prevalent may indicate arthritis associated with Lyme disease Recent joint surgery Previous intra-articular corticosteroid injection Sexual activity - risk of gonococcal infection cause of arthritis
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septic arthritis presentation
typical triad: low grade fever, pain and impaired range of motion in one joint. Hot, swollen, tender and acutely painful single joint Presents for <2 weeks Restricted movement; painful with movement Fever Usually in larger joints Common in prosthetic joints Initial history of erythema migrans, migratory joint pain and later intermittent oligoarthritis usually involving the knee or large joints may suggest lyme arthritis Bacteraemia: prostration, vomiting or hypotension Prosthetic joint: may show less of these typical signs more likely to present later with drainage sinus, abscess around the joint (painful) and loosening of implant (painful) young, fit with history of STI, poly arthritis and skin lesions likely gonococcal arthritis sternoclavicular and sacroiliac joints most likely caused by group B streptococcal infection
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investigations of septic arthritis
treat a hot, swollen acutely painful joint with restricted movement as septic arthritis until proven otherwise; even in absence of fever Synovial fluid sample (DO NOT ASPIRATE PROSTHETIC JOINT; refer to ortho surgeon; CI for skin infection or heavily colonised skin eg psoriatic plaques) for culture and sensitivities and white cell count (leukocyte count, gram staining, polarising microscopy for crystal arthropathy and culture for causative organism) Bloods and blood cultures and sensitivities (FBC increased WCC, ESR and CRP) Procalcitonin - rises sharply in bacterial endotoxin presence (usually <0.1ng/mL) MRI/CT most sensitive imaging reserved for diagnostic difficulty Synovial fluid PCR (reactive arthritis and causative organisms) Swabs for culture and sensitivity Calprotectin - not yet shown useful enough for routine practice but could potentially help differentiate between septic and aseptic arthritis If lyme disease is suspected but NO rash present: blood sample for testing. If rash: treat as lyme disease Swab of urethra, cervix and anorectum if gonococcal infection suspected
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management of septic arthritis
First line follow sepsis protocol (NEWS score; sepsis 6 if indicated) Analgesia (NSAIDs) and splint limb in position of function (eg knee in extension, elbow at 90 degrees etc.) once infection is under control (lab markers and symptoms) immediate joint mobilisation to avoid contractures Take synovial fluid samples and send for culture and sensitivities Empirical antibiotics in suspected native joint non systemic involvement and aspirate joint (flucloxacillin, clindamycin for allergy, vancomycin for MRSA, cefotaxime/ceftriaxone for gonococcal) Once confirmed change antibiotics to specific sensitivity if needed; continue antibiotics IV for 2 weeks unless lack of response then 4 weeks oral antibiotic therapy Consider ortho/surgery referral for evacuation of pus Refer prosthetic joints to orthopaedics (consider surgery) Refer to orthopaedics for USS joint aspiration if joint is inaccessible
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gonococcal arthritis
Most common cause of septic arthritis in previously fit young adults Can be secondary to genital, rectal or oral gonorrhoea which is often asymptomatic Organism detected in swab cultures and blood cultures/synovial fluid cultures Treatment is with Cefotaxime or Ceftriaxone for 2 weeks and joint rest Usually presents as dermatitis arthritis syndrome Polyarticular arthritis (fever, arthralgia) sometime monoarticular arthritis Tenosynovitis of hands, knees, wrists, ankles and elbows Multiple skin lesions (maculopapular pustules)
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prosthetic joint infection and viral joint infection presentation
Prosthetic joint infection: May present very late after several months Often no signs of significant swelling or fever Presents as prolonged gradually increasing pain Cellulitis and sinus often develop also Viral arthritis Eg rubella, parvovirus, HCV, HIV Symmetrical involvement of small joints like tha hands Rash often present
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TB septic arthritis
Symptoms may be indolent and diagnosis may be delayed for many years Hip, knee and spine most commonly affected Insidious onset of pain, swelling and dysfunction ‘Boggy’ joint on palpation due to granulomatous involvement Patient is febrile with night sweats and weight loss Culture of synovial fluid, synovial biopsy needed to diagnose Treatment as for TB but extended to 9 months along with joint rest and immobilisation then mobilisation with recovery
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Lyme disease arthralgia
Caused by borrelia burgdorferi Presentation: Swelling disproportionate to pain level History of tick bite or travel to endemic areas Transient polyarthralgia (not arthritis) Erythema migrans Systemic symptoms Joint inflammation may present months after initial infection and commonly affects large joints like the knee Investigation - no conclusive tests for lyme disease (clinical diagnosis, blood test which often negative early on anyway) Treat anyone with typical presentation and rash immediately for lyme disease Suspected but no rash - blood sample and refer to lyme disease diagnostic services for rare and imported pathogens lab testing (antigen testing PCR)
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Paget disease of bone
Can also get Paget’s disease of nipple/breast Paget disease of bone leads to thickened skull, inner and outer bony tables fused, OA of hip, bowing of tibia Cause is unknown Rare in under 40s, incidence increases with age More Common in temperate climates and in anglo-saxons Pathology: Increased bone turnover with increased numbers of osteoblasts and osteoclasts increasing bone remodelling Phases: lytic, mixed (lytic + blastic), sclerosis (disorganised new bone formation) Bone enlargement, deformity and weakness Paget bone is larger, deformed, weaker and more at risk of cancers
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Paget disease presentation
Asymptomatic 70% Deep boring pain Bony deformities and enlargements of skull, lumbar spine, pelvis, femur and tibia most commonly Tibia: bowed sabre tibia (bow legs) Skull: lion like face (leontiasis), frontal bossing of skull, enlarged maxilla and increased head size Kyphosis of spine Pelvic asymmetry XR lesions can resemble glass shard or blade of grass or candle flame shows osteoporosis in osteolytic phase of disease skull can show cotton ball appearance in intermediate phase of disease osteosarcoma can be complications
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complications of Paget disease
Pathological fractures Osteoarthritis Nerve compression: pain, hearing loss, vision loss, root compression (cauda equina syndrome, lower limb muscle weakness) High output HF if >40% skeleton is involved Hypercalcaemia Osteosarcoma (Paget sarcoma) after >10 years <1% show sudden onset worsening of chronic bone pain but still 30x more common than normal population!
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Paget disease investigations
diagnosis confirmed with XR features, high ALP and bone biopsy Clinical presentation: sabre tibia XR in axial skeleton showing enlargement, patchy cortical thickening, sclerosis, osteolysis, deformity, blade of glass lesion (V shaped pattern between healthy and diseased bone), cotton wool pattern in skull (multifocal sclerotic patches) Bone scan (DEXA) for hot spots of growth Bloods: hypercalcaemia, PO4 normal, PTH normal, increased ALP from osteoblastic action (LFTs), urinary hydroxyproline increased = collagen destruction, U+Es, eGFR, FBC (infections) Bone biopsy to rule out tumours
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management of Paget disease
Orthotic devices: walking sticks, walkers Calcium and vitamin D increased intake/supplementation Surgical repair for deformity, compressions of nerve, pathological fractures or cancers Monitor for signs of osteosarcoma (presentation increased bone pain, local swelling, pathological fractures)
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sickle cell anaemia
Autosomal recessive Most common in african descent; must screen all african origin people for SCD pre-op 1/700 incidence HbSS - homozygotes (SS) symptomatic sickle cell anaemia HbAS - heterozygous - sickle cell trait (no symptoms but falciparum malaria resistant) may still experience symptomatic sickling hypoxia Pathology: Results from three interconnected sequelae of SCD Vaso-occlusive crisis results in bone infarcts and subperiosteal haemorrhages Chronic anaemia resulting in expansion of medullary spaces Infection These predispose individuals to complications such as growth disturbance and pathological fractures ``` Pathogenesis: Hypoxia Deoxygenated HbS Polymerises Deformity of RBCs, sickle cells cannot travel normally or carry oxygen Haemolysis + blocked small vessels ```
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sickle cell disease investigations
Bloods: Hb 60-90g/L, reticulocytes 10-20%, high bilirubin. Haemolysis variable Film: sickle cell and target cells Sickle solubility test +ve but doesn't distinguish between types Hb electrophoresis confirms diagnosis radiographic features of SCD: Vaso-occlusive crisis shows osteonecrosis, subperiosteal and epidural haemorrhage, hand-foot syndrome (dactylics) and growth disturbance infection shows osteomyelitis chronic anaemia shows marrow hyperplasia
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vaso-occlusive painful crisis/sickle cell crisis overview
Commonly occurs from microvascular occlusion causing distal ischaemia Can be triggered by cold, dehydration, infection or hypoxia Associated with dehydration and raised haematocrit Symptoms typically include pain, fever, those of triggering infection Bone marrow infarction causes severe skeletal pain; osteomyelitis presents with localised pain and systemic features of infection Hands and feet show dactylitis (inflammation of finger or toes) Mesenteric ischemia results in acute abdomen presentation CNS infarction results in stroke, seizures, cognitive defects Splenic infarction - susceptibility to infection (40% SCD childhood deaths) Poor growth, chronic renal failure, gallstones, retinal disease, iron overload Lung damage from hypoxia causing fibrosis and pulmonary HTN Can cause priapism in men by trapping blood in penis causing painful and persistent erection (urological emergency treated with aspirin of blood from penis) Management: IV opiates, haematologist advice, G+S bloods, FBC, reticulocyte count, septic screen (Blood cultures, MSU + CXR), rehydrate and keep warm, oxygen PRN, consider empirical antibiotics if fever >38, unwell or chest signs
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hand foot syndrome overview
Occurs in 50% children with SCD Most common between 6 months and 6 YO Usually have systemic symptoms of fever, elevated WCC Characterised by swelling of hands and feet (uni or bilateral) Usually self limiting
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sickle cell disease management
Cord blood taken at birth Pneumococcal prophylaxis (vaccine +/- penicillin V) Referral to hematologist for chronic management Prevention: genetic counselling, parental tests and education can prevent 90% deaths form crisis crisis management: IV opiates, haematologist advice, G+S bloods, FBC, reticulocyte count, septic screen (Blood cultures, MSU + CXR), rehydrate and keep warm, oxygen PRN, consider empirical antibiotics if fever >38, unwell or chest signs
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types and general presentation of metabolic bone diseases
``` types: osteoporosis osteomalacia vitamine D déficient (rickets) renal osteodystrophy paget disease fibrous dysplasia ``` ``` presentation: deformities bone pain height loss due to vertebral compression pathological fractures associated abnormalities in some of them ```
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renal osteodystrophy (CKD-MBD)
Spectrum of disease seen in patients with chronic renal disease Characterised by bone mineralisation deficiency due to electrolyte (Ca and PO4) and endocrine (PTH) abnormality Common cause of hypocalcemia Renal failure leads to 1,25 dihydroxy-cholecalciferol deficiency (active form of vitamin D) Pathology: Hypocalcemia: due to inability of kidney to convert vitamin D3 to calcitriol (active form) because of Phosphate retention (hyperphosphatemia) Hyperparathyroidism and secondary hyperphosphatemia caused by hypocalcaemia and lack of phosphate excretion by damaged kidney Uraemia related phosphate retention results
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renal osteodystrophy presentation
anaemia: pallor, lethargy, Sob with exercise platelet abnormality: epistaxis, bruising skin: pigmentation, pruritus GIT: anorexia, nausea, vomiting, diarrhoea endocrine/gonads; amenorrhea, erectile dysfunction, infertility polyneuropathy CNS: confusion, coma, fits (severe uraemia) CVS: uraemic pericarditis, HTN, peripheral vascular disease, HF renal: nocturne, polyuria, salt and water retention oedema renal osteodystrophy: osteomalacia, muscle weakness, bone pain, hyperparathyroidism, osteosclerosis, dynamic bone disease
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renal osteodystrophy investigations
XR: subperiosteal bone erosion/reabsorption, chondrocalcinosis at knees and pubic symphysis, osteopenia, pathological bone fractures, pseudofractures (Looser’s zone), brown tumours BMD - osteopenia Pseudofractures (Looser zone) is a diagnostic finding osteomalacia. Rare in Paget’s disease of bone, hyperparathyroidism, renal osteodystrophy, osteogenesis imperfecta, fibrous dysplasia and hypophosphatasia. Band of bone material of decreased density may form alongside the surface of the bone. Thickening of the periosteum occurs and formation of callouses in affected areas is also common. Gives the appearance of a false fracture
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management of renal osteodystrophy
CKD management Management of hyperphosphatemia: dietary phosphate restriction, oral phosphate-binding agents (such as calcium carbonate, sevelamer or lanthanum carbonate) Vitamin D analogues (such 1alpha cholecalciferol or vitamin D metabolite 1,25-dihydroxyvitamin D3) Bisphosphonates if indicated for prevention and treatment of osteoporosis
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bursitis
Inflammation of the small fluid filled sacs found around joints/mobile areas in the body Inflammation leads to increased synovial fluid production and causes swelling Prepatellar bursa are the most commonly affected (located superficially on anterior aspect of the knee between skin and patella) Classification: Non-septic: sterile inflammation of bursa. On infectious causes include trauma, overuse, gout, systemic disease Septic: infection of bursal sac with microorganisms. Complications include septic arthritis, skin infection, necrosis, osteomyelitis and sepsis Causes: Acute trauma: fall/direct blow to knee Recurrent minor injuries: after long periods of time spent kneeling or pressure on patella (Housemaids knee) Infection: pyogenic prepatellar bursitis is common in children. May be mistaken to septic arthritis History of preceding trauma or disease: previous traumatic bursitis, RA or gout
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bursitis presentation
``` (prepatellar bursitis): Knee pain, swelling Difficulty kneeling and walking Fever Tenderness Localised erythema and warmth Normal range of joint movement (but slightly reduced) Systemic signs of fever, tachycardia may indicate septic bursitis ```
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bursitis management
Aspiration of bursae for culture and analysis XR; MRI; USS to exclude fractures or soft tissue injury or monitor treatment Non-infective: Analgesia, rest, protection (knee pads/cushions) Physiotherapy Education on prevention Aspiration and steroid injections after excluding septic bursitis Referral to orthopaedics if chronic or recurrent for arthroscopic bursectomy Septic bursitis: Aspiration to confirm diagnosis Antibiotics therapy whilst waiting for culture conformation Incision and drainage if symptoms do not improve significantly within 36-48 hours of antibiotics
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meniscal tear
Fibrocartilage C shaped pads that deepen the articular surface of the tibia increasing joint stability and act as shock absorbers as well as lubricate joint Meniscus tears usually occur through twisting or pivoting force in young active people. Can be torn causing degenerative tear with very minimal force in middle aged and elderly people Mainly either traumatic or degenerative MRI considered most accurate and non-invasive diagnosis Most tears do NOT spontaneously heal and are treated arthroscopically by meniscus repair if torn in clear pattern but not considered for those with large >1cm meniscus tears or root tears
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meniscal tears presentation
Acute sudden pain usually following trauma Popping, catching or locking (usually in flexion) Buckling Joint pain and tenderness May be unable to fully extend or flex knee Knee swelling (slow onset over 3-36 hours due to effusion; if rapid, suspect bleeding or other ligament injury Meniscal tears often associated with ACL injury due to being connected *McMurrary test NO LONGER recommended due to causing potential further damage*
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meniscal tear management
PRICER Protect from further injury Rest (crutches for initial 24-48 hours) Ice for 20 min periods of each waking hour during initial 48 hours Compression with brace or splint if needed Elevation Rehabilitation: physiotherapy exercises Urgent referral to orthopaedics if knee is locking or severe injury Surgical repair
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Chondromalacia patella overview
Softening of the cartilage of the patella usually as a result of indirect/direct trauma e.g. in athletes or degenerative changes Significant cause of anterior knee pain in females, tall or obese people Causes retropatellar pain worse on rising from prolonged sitting or using the stairs (especially walking downstairs) or when squatting Physical examination: Posterior surface of patella can be felt if pushed sideways Often tender If the patella is pressured against the femur and then moved this causes pain Crepitus can be heard swelling Diagnosis: Clinical MRI to assess cartilage and exclude other ligament injuries Management: Simple analgesia (NSAIDs) Physiotherapy: home exercising program to stretch, straighten and semi-squats Arthroscopic surgery (chondroplasty to smooth damaged cartilage on back of patella)
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slipped upper femoral epiphysis
Weakness in proximal femoral growth plate (physis) leads to displacement of the capital femoral epiphysis The metaphysis that displaces anteriorly and superiorly leading to the slipped state Presents as pain and limp Acute form (10-15%) slippage occurs suddenly, normally spontaneously Chronic (85%) steadily progressive slippage is the most common form Typically seen in adolescent aged 10-13 years External rotation on hip flexion is key examination finding Classified as stable 90% (can walk) or unstable 10% (can’t walk) Unstable is high risk of osteonecrosis Temporal classification is based on duration of symptoms but rarely used. Acute <3 weeks, chronic >3 weeks and acute on chronic is acute exacerbation of long standing symptoms
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risk factors for slipped upper femoral epiphysis
Mechanical: local trauma, obesity (80%) Hormonal: testosterone weakens physis (more common in males) Hypothyroidism Radiotherapy and chemotherapy to hip
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pathology and presentation of slipped upper femoral epiphysis
Pathology: Factors all induce stress around the hip joint and apply shear force at the growth plate. Growth plate is intrinsically weak, excess weight, stress of growth spurt and changing hormonal levels shift the metaphysis anteriorly and superiorly Presentation: Usually unilateral (contralateral slip in 40-50%) Discomfort in hip, groin, medial thigh or knee (referred) during walking Limp Pain accentuated in running or jumping Acute (<3 weeks) show severe pain resulting in inability to walk or stand Hip motion is limited especially internal rotation and abduction due to pain When flexed the hip tends to externally rotate Mild-moderate shortening of the affected leg in chronic cases
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diagnosis of slipped upper femoral epiphysis
clinical XR: Klein line drawn along femoral neck on AP XR should pass through lateral margin of femoral head (arrow). if the upper femoral epiphysis has slipped the line does not trethowan's sign: semilunar head (more acute angle) of femur rather than larger more circular normal head of femur in normal position
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management of slipped upper femoral epiphysis and complications
Avoid moving or rotating leg (immobilize) Do not allow walking Analgesia and immediate orthopaedic referral if suspected Surgery is standard treatment to stabilise joint via percutaneous pin fixation ``` Complications: Excellent prognosis 91-95% cases when slip is mild-moderate Avascular necrosis of epiphysis Chondrolysis (degeneration of cartilage) Osteoarthritis of hip Recurrence of progression ```
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bone cysts
Aka simple bone cysts Common benign non-neoplastic fluid filled lesions Rare before age 3 and after skeletal maturity Usually present pathological fractures (asymptomatic before then) following relatively minor trauma, normally involving proximal humerus or femur Treatment is to allow fracture to heal and then aspirate and inject with either methylprednisolone or bone marrow Usually gets smaller over time and self resolves
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bone cysts management and prognosis
Asymptomatic lesions requires no intervention If large and threatening to fracture or cause deformity then intralesional steroid injection can be performed If fractured bone this normally heals on its own (with immobilisation) Surgery with curettage and bone grafting is sometimes required (few cases)
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aneurysmal bone cyst
Usually presents before age 20 with pain and swelling Cavernous spaces filled with blood and solid lumps of tissue Mainly affect the femur, tibia and spine which may lead to cord or nerve root compression resulting in neurological symptoms Grow rapidly and may be confused with malignancy (confirm with biopsy) Treated with curettage/bone grafting or excision Recurrence in 20-30% usually in the first 1-2 years after treatment and mainly in younger children
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scaphoid fracture overview
The most frequently fractured carpal bone (70-80%) Usually fall onto outstretched hands, common in contact sports Occurs most commonly in adolescents and young adults Tender anatomical snuff box and circumduction of wrist can be painful Tender thenar eminence Pain on axial loading of thumb Initial radiograph can miss 5-20% fractures in acute setting Major complication is non-union/malunion leading to instability and secondary osteoarthritis change or avascular necrosis which is directly correlated with proximity of fracture to proximal pole Imaging needs scaphoid series of XR for best view (four projections of scaphoid to look for fracture/displacement, scaphoid fat pad sign and associated scapholunate ligament disruption) Terry Thomas sign can be accentuated with clenched fist (increased scapholunate space on AP radiograph of wrist or coronal CT usually >3/4mm) Can also use MRI, USS, CT etc. to assist diagnosis Treatment may need prolonged period of cast immobilisation in short arm or thumb spica cast, percutaneous surgical fixation or microsurgical graft reconstruction Splint for small fracture or cast for larger fractures Surgical treatment of displaced fractures or angulation
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colles fracture overveiw
Most common type of distal radial fracture seen in all adults, particularly in those with osteoporosis Mostly secondary to fall on outstretched hands with pronated forearm in dorsiflexion Proximal row of carpus (particularly lunate and scaphoid) transfer energy along distal radius meaning most fractures are dorsally angulated and impacted If dorsal angulation is severe enough a DINNER FORK deformity (bayonet deformity) is seen due to malunited Colles fracture Also usually impaction with resultant shortening of radius Associated ulna styloid fracture present in 50% cases Management: Majority treated with closed reduction and cast immobilization Cast extends from below elbow to metacarpal heads and holds wrist somewhat flexed in ulnar deviation Closed reduction and casting immobilisation Open reduction and internal fixation (ORIF) considered when the fracture is unstable or unsatisfactory closed reduction is achieved
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smith's and barton's fracture
Extra articular transverse fractures often referred to as reverse colles fracture <3% all radial and ulnar fractures Usually occur via either falling onto flexed wrist or direct blow to back of the wrist Extend through dorsal aspect to articular surface but not to volar aspect Usually associated dorsal subluxation/dislocation of radiocarpal joint Reverse Barton fracture is a type II Smith fracture
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Monteggia fracture-dislocation
Fracture of ulna shaft (usually obvious) with dislocation of the radial head (often overlooked) Typically occur as result of fall onto outstretched hands Mostly occur in children ages 4-10 and rarely in adults
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management of distal radius/forearm injury
nondisplaced/minimally displaced distal radius fracture - splint/BE back slab and follow up in fracture clinic Displaced fracture without features - manipulation, backslab, re-XR and fracture clinic follow up High energy injury/open fracture/neurological deficit/fracture highly displaced/grossly unstable fracture - sedation in ED + manipulation by orthopaedics and orthopaedic referral Isolated ulna shaft fracture - above elbow backslab and fracture clinic follow up Forearm fracture, monteggia fracture-dislocation, galeazzi fracture dislocation - above elbow backslab and orthopaedic on call referral *A 'back slab' is a slab of plaster that does not completely encircle the limb and is used for injuries which have resulted in a large amount of swelling. It is secured with a bandage to accommodate the swelling. This type of plaster is only temporary and will probably be 'completed' at your Fracture Clinic appointment.*
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mechanism of injury in elbow fractures and dislocations
radial head and neck fractures - fall onto outstretched hand olecranon fractures - elderly; indirect trauma by pull of triceps and brachioradialis. children; direct blow to elbow fractures of coronoid process - fall onto extended elbow as for elbow dislocation fractures of distal humerus - fall on to extended outstretched hand intercondylar fracture - direct or indirect blow to elbow condylar fracture - direct blow to flexed elbow capitellum fracture - fall onto outstretched hand or direct trauma elbow dislocation
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positive fat pad on XR (elbow)
With joint effusion (fluid/pus/blood) or synovitis the capsule will become distended Fat pads are located anteriorly and posteriorly of distal humerus When effusion becomes large enough the fat tissue can be displaced away from humerus (positive fat pad) In trauma setting this almost always indicates a fracture particularly in adults (less specific in children as soft tissue damage may be associated with joint effusion)
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elbow lunation
Fall onto outstretched hands with elbow in HYPERextension may cause this Virtually always a posterior luxation: olecranon is posterior of the humerus Regularly associated with fractures, particularly of the radial head and coronoid process Combination of posterior elbow luxation, radial head fracture and coronoid process fracture are termed the terrible triad
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elbow fractures
Supracondylar - distal humerus fracture: Supracondylar fractures in children must be reviewed by an ED senior registrar or consultant to look for any angulation or displacement, swelling can cause neurovascular compromise and therefore needs referral to an orthopaedic on call team. If definitely no angu;ation or displacement then can discharge home medial epicondylar fracture
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pulled elbow
Common in children particular 2-3 YO suddenly pulled by the arm when it is in extension Radial head becomes subluxated Child holds elbow in flexion and pronation and refuses to extend elbow Radial head if fixed by the annular ligament but in this injury it causes subluxation of radial head under the ligament Clinical diagnosis of typical presentation and history not usually needed to XR Treatment is reduction - pronation/supination movements of the forearm causes radial head to return to anatomical position (sometimes clicks) can use supination flexion manoeuvre - pronate arm in extension; then both supinate and flex forearm to put ligament back over radial head child should feel immediately better and be able to move the limb normally/play normally if no improvement soon after consider alternate diagnosis
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shoulder dislocations
Most commonly dislocated joint Subluxed: parietal dislocation. Dislocation = full dislocation. Both cause pain and unsteadiness of joint Anterior shoulder dislocation is most common (95%) but can also have posterior and inferior dislocations. Anterior dislocations can tear the shoulder capsule and detach the labrum from the glenoid fossa and a fracture of the humeral head/neck/greater tubercle can occur at the same time Usually results from forced abduction, external rotation and extension The shoulder is in its most vulnerable position Patient presents with severe pain and restricted movement of shoulder, majority present following trauma to shoulder Ix: shoulder XR series (AP and Y view) can also use CT, MRI etc. Assess for axillary nerve damage: check sensation on lateral aspect of shoulder on deltoid muscle (Sergeants stripe) Radial nerve: thumb, wrist, elbow extension and sensation on dorsum of hand A flattened, shallow anterior/anterior inferior glenoid bony contour may predispose to recurrent dislocation Only treatment is prompt reduction of the shoulder joint usually done in A+E following sedation and analgesia Should splint the shoulder in abducted position when found, place pillow/barrier in space between arm and chest for support, flex elbow to 90 degrees and sling given for support.
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neck fracture and dislocations and XR rules
Cervical spine susceptible to injury as it highly mobile with relatively small vertebral bodies and supports large weight C2 and C7 are most commonly fractured Children have a different fulcrum of movement than adults especially at C2/3 compared to C5/6 making them more vulnerable to cervical fracture ``` Canadian C spine rules for XR: HIGH RISK: 65, fast drive, sense deprive (imagine if alive) - >65 YO - dangerous mechanism - paraesthesia in extremities ``` ``` LOW RISK: slow wreck, slow neck, sitting down, walking round, C spine fine (range the spine) - spine rear end MVCC - delayed neck stiffness or pain onset - sitting position in ED - ambulatory at any time - absence of midline C spine tenderness ``` are they able to rotate neck 45 degrees left and right? if no - XR if none of the above - DONT XR
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wedge/compression fractures
Hyperflexion injuries resulting from axial loading Most commonly affecting anterior aspect of vertebral body Most common type (50%) of thoracolumbar spine fractures Typically are secondary to osteoporosis although some are secondary to focal bone lesion Small portion from trauma in those with no underlying bone disease Most patients with osteoporotic compression fractures there is no neurologic injury but only pain from the fracture
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burst fracture
Type of compression fracture related to high energy axial loading spinal trauma results in disruption of posterior vertebral body cortex with retropulsion into spinal canal Usually present as back pain and/or lower limbs neurologic deficits in clinical scenario of trauma Burst fractures most commonly occur at L1 with majority occurring from T9-L5 Two level burst fractures are less common than single Typically they occur following a fall from height (often landing on feet) or from motor vehicle accident General features: Loss of vertebral height on lateral views: anterior portion commonly compressed more than posterior Fracture always involved posterior vertebral body cortex Burst vertebral body on axial CT Vertical fracture through posterior elements is usually present in more severe trauma Interpedicular widening Bone fragment retropulsion into spinal canal may occur and needs MRI to determine
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Jefferson fracture
Eponymous fracture is name given to a burst fracture of the atlas Caused by axial loading of cervical spine resulting in occipital condyles being driven into lateral masses of C1 Often associated with head injuries and other concurrent cervical spinal injuries Not normally associated with neurological deficit although spinal cord injury may occur if there is retropulsed fragment Usually unstable and account for ⅓ of all C1 fractures Gehweiler classification describes injuries of the atlas with a burst of type 3 injury defining the pattern seen in a Jefferson fracture Ix: XR, CT, MRI Treatment usually conservative (hard collar immobilisation) as long as the transverse atlantal ligament is intact (no widening of atlantodental interval or MRI intact visualisation) If disrupted or unstable injury then halo immobilisation needed, posterior C1/2 lateral mass internal fixation or transoral internal fixation
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odontoid peg fracture
Common cervical fractures mostly in elderly patients Mechanism is variable can be via flexion or extension with or without compression Two classifications: Anderson and D’alonzo (most common and describes level of fracture line) and Roy-Camille which has been shown to better correlate with prognosis and describes plane of fracture and displacement Present following low impact injuries with neck pain Can be fatal with significant displacement of odontoid Those who survive can have no neurological pathology
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traumatic spinal cord injury
Leads to damage of spinal cord resulting in temporary or permanent change to neurological function including paralysis More common in males and majority are from preventable cases such as falls, road traffic collisions or sport injuries Classified as incomplete or complete Complete is damage occurring across whole spinal cord width leading to complete loss of sensation and paralysis below injury level Incomplete is spread across part of spinal cord thereby only partially affecting sensation and movement below injury Pathology: Initial acute impact resulting in concussion on spinal cord OR compression on spinal cord from increased pressure from nearby rigid structures (vertebrae and discs) which may have been displaced in injury This increases tissue pressed and can block venous return resulting in oedema around spinal cord Arteries can also be compromised leading to spinal cord ischaemia which causes spinal cord nerve damage (gliosis) Classification by pathology: Primary from destructive forces that directly damage neural structures like shear forces tearing an axon or direct compressive force occluding blood vessels causing ischaemia Secondary from injury cascade
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traumatic spinal cord injury grading
A - complete - no motor or sensory function preserved in sacral segments S4-5 B - sensory incomplete - motor function not preserved below neurological level and includes sacral segments S4/5 while sensory function is preserved C - motor incomplete - motor function preserved below neurological level; more than half of key muscles below neurological level have muscle grade <3 D - motor incomplete - motor function persevered below the neurological level; at least half of key muscles below neurological level have muscle grade >3 E - normal - motor and sensory function normal
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presentation of traumatic spinal cord injury and investigations
Clinical features depend on the level and completeness of injury, and around 10% of traumatic spinal injuries will result in tetraplegia or paraplegia. Pain may not be present in every case. Clinical signs can include loss of motor function, loss of sensory function, bowel incontinence, or urinary incontinence. The ASIA Impairment Scale can be used to classify the degree of injury to the spinal cord following spinal injury Investigations: Immobilize cervical spine ALWAYS History for mechanism of injury XR/CT/MRI XR first line for suspected spinal injury without abnormal neurological signs CT if suggestive of spinal column injury If spinal column fracture confirmed image the rest of the spinal column
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traumatic spinal cord injury management
Discuss with neurosurgical or spinal team Management guided by displacement, stability and associated neurological deficit of injury and in absence of these can be managed conservatively usually Bed rest, cervical collars, motion restriction devices and traction followed by early mobilisation and rehabilitation Surgery needed if there is evidence of progressive neurological deficit or dislocation type injury (displaced and unstable) Cervical spine surgery aims to realign the spine, decompress the neural tissue, and stabilise the spine with internal fixation (screws, plates, cages) Thoracolumbar spine surgery typically involves spinal decompression, discectomy, spinal fixation, or spinal cord stimulation Studies have shown earlier surgical intervention (within 24 hours) is associated with better outcomes. Physiotherapy and other specialist therapy input (e.g. speech and language or occupation therapy) should be utilised early (as soon as deemed safe), as TSCI patients often require extensive rehabilitation both as inpatient and outpatient. Goals of therapy need to be discussed with the patient, to build a realistic rehabilitation plan.
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knee fracture
Patella: accounts for 1% of all fractures, most common in ages 20-50. ➤ Femoral condyles: these usually fracture when the knee is stressed. ➤ Tibial eminence: caused by accidents, such as a blow to the proximal tibia when the knee is flexed, or if the knee is hyperextended during an accident. Usually seen in patients aged 8-14 Tibial tuberosity: more common in men than in women, and in younger patients rather than adults; often seen in athletes, especially those involved in jumping sports. Tibial plateau: compressive fractures of the articular surface, typically from extreme force such as fall from a height or being hit by a vehicle, although in patients with osteoporosis minimal force may be needed. Segond's fracture: this is an avulsion fracture of the lateral tibial condyle immediately beyond the articular surface with the knee. Although not directly a part of the knee joint, it occurs in association with tears of the anterior cruciate ligament (ACL), medial meniscus and lateral capsular ligament, and is thus included here
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patella fracture management
Around 1% all fractures and are most common in those aged 20-50 YO ⅔ are male Present with swelling and pain over the patella with point tenderness and marked reduction in extension strength Usually there is a large joint effusion or haemarthrosis Complications include stiffness, weak extensor mechanism and degenerative disease of patellofemoral joint Causes: direct blow to patella (dashboard injury), severe force by extensor mechanism, after ACL reconstruction or total knee reconstruction or pathological fracture Transverse fracture of mid patella is most common, vertical fracture is least common Other types: undisplaced, lower/upper pole fractures, comminuted, comminuted nondisplaced and osteochondral Treatment: determined by amount of displacement and if extensor mechanism is intact or disrupted Those with minimally or nondisplaced fracture and intact EM may have conservative management (Zimmer knee splint for 4-6 weeks can usually weight bear while splinted) If displaced or disrupted EM surgical management (K wiring) usually needed
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Boxers fracture overview
Neck of 5th metacarpal fracture Minimally comminuted, transverse fractures Most common type of metacarpal fracture Impaction injury almost always caused by direct blow with clenched fist against solid surface causing axial loading of the 5th metacarpal Most commonly male injury In most cases the neck fracture is transverse orientated and minimally impacted with volar angle Spiral fracture or angulation can sometimes occur Degree of angulation best assessed on lateral XR Can be treated conservatively however often are relatively unstable and K wire fixation often needed (closed reduction and internal fixation) Short arm gutter splint applied with flexion of MCP joint for 2-3 weeks followed by buddy strapping (avoid prolonged immobilization as can lead to stiffness Fractures of the 4th metacarpal neck are treated similarly while 2nd and 3rd usually need internal fixation
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Gamekeeper/Skiers thumb overview
Avulsion or rupture of ulnar collateral ligament of the first MCP joint Skier’s thumb refers to acute trauma from hyperabduction of the thumb as it is caught by a ski pole strap Gamekeeper’s thumb refers to chronic non-traumatic overuse injury (stress and repetitive trauma) that gradually injures the ulnar collateral ligament UCL may partially rupture partially or completely or may avulse off it’s bony attachment Distal attachment site to proximal phalangeal base is the most common avulsion site XR or USS can be useful to identify fracture or ligament damage or MRI Conservative treatment given usually Surgical treatment for those with joint instability, displaced avulsion fracture or presence of stener lesion
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how to measure ulna and radial fractures
Most forearm fracture include fracture of distal radius as well as ulna fracture (60%) In some cases there is associated dislocation of one bone with fracture of another Distal radius parameters Radial height: normally 9.9-17.3mm (<9 indicates impacted fracture of radial head) Radial inclination: agle of distal radial surface with respect to line perpendicular to shaft. Normal should be 15-25 degrees Volar tile (lateral): angle of distal radial surface with respect to line perpendicular to shaft. 10-25 degrees is normal. Negative angle indicates dorsal angulation Ulnar variance: height of ulnar with respect to radial articular surface. Normally 9-12mm
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radial head lunation and elbow lunation
Radial head luxation: Lateral head of radius is dislocated and articulation with ulna and humerus is abnormal Radiocapitellar line no longer runs through central capitellum Elbow luxation: Fall onto outstretched hands with elbow in HYPERextension may cause this Virtually always a posterior luxation: olecranon is posterior of the humerus Regularly associated with fractures, particularly of the radial head and coronoid process Combination of posterior elbow luxation, radial head fracture and coronoid process fracture are termed the terrible triad
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greenstick fracture
Incomplete fractures of long bones usually seen in young children, more commonly less than 10 YOs Commonly mid-diaphyseal affecting the forearm and lower leg Occur when force is applied to a bone resulting in bending of the bone such that the integrity of the cortex has been overcome results in fracture of the convex surface However the bending force does NOT break the bone completely and the concave surface of bent bone remains in tact This can occur following an angulated longitudinal force applied down the bone (e.g. an indirect trauma following a fall on an outstretched arm), or after a force applied perpendicular to the bone (e.g. a direct blow). Much less common than torus fracture XR features: usually mid-diaphyseal, in tandem with angulation and incomplete fracture with cortical breach of only one side of bone
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torus fractures
Incomplete fractures of the shaft of a long bone that is characterised by bulging of the cortex Results from trabecular compression due to axial loading force along long axis of the bone Usually seen in children ages 5-10 frequently involve the distal metaphysis Strictly speaking refers to a circumferential buckle fracture Pathology: axial loading on bone. Eg falling onto outstretched arm XR features: no fracture lines seen distinctly, subtle deformity or buckle of cortex may be evident and in some cases angulation may be only diagnostic clue In children <7 YO a distance of <1 cm between fracture and physis means a potentially unstable distal radius and is more likely than a buckle fracture Usually self limiting and do not need surgical intervention although manipulation may be needed if angulation is severe Sometimes case and splint is all that is needed with rest and immobilization before moving
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Shoulder fractures
Humeral head fractures: Proximal humerus fractures are common often seen in elderly with ostoeporotic bone following simple ground level fall on outstretched arm Sling immobilisation is main treatment Surgical treatment indicated for more complex and displaced fractures Humeral fracture: Proximal, midshaft and distal humeral fractures Spiral, transverse Distal humeral shaft spiral fracture Acromioclavicular joint injury: Underside of acromion should align with underside of distal clavicle if it does not it’s probably a dislocation Dislocation treated with ministry sling Diagnose with ACJ XR series AC joint is tender but XR normal = sprain Increased in costocervical distance >100% skin tending associated injuries = surgery
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hangman fracture
Aka traumatic spondylolisthesis of axis is a fracture through the pars interarticularis of C2 bilaterally usually with subluxation of C2 vertebra on C3 Caused by cervical hyperextension and distraction (historically forces delivered by noose, but virtually never seen in suicidal hanging) Presents post traumatic neck pain and neurological impairment seen in 25% patients Can be unstable and surgical fixation needed in these cases Treatment is bracing or more typically internal fixation
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femoral fractures
Prayer’s fracture: Insufficiency fracture of posterior femoral condyle Typically occurs secondary to prolonged repeated knee flexion placing force on the non-weight bearing posterior condyles, such as that encountered with daily prayer ritual where knee is held in extreme flexion Chondral fracture: Fractures involving the cartilage only (unlike osteochondral fractures which involve both articular cartilage and subchondral bone plate) Commonly from rotational injury or direct blows leading to chondral defect with fragment of bone remaining in situ, displaced and loose Typically occur in combination with ligamentous injuries in young adults but can be seen in isolation in adolescents Presents variably, depending on extent and associated injuries (pain, limited motion, locking, clicking and swollen joint) may have dislocations if ligament damage Not easily detected on plain XR or CT best seen on MRI Treated arthroscopically or operatively (rescue and fixation technique)
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patella dislocation
Lateral displacement follow by dislocation of the patella due to disruptive change to the medial patellar retinaculum Accounts for around 3% all knee injuries and commonly seen in those participating in sports Most commonly caused from twisting motion with knee in flexion and femur rotating internally on fixed foot (valgus flexion external rotation) XR shows laterally displaced patella, joint effusion and silver sign (curvilinear intra articular osteochondral fragment in knee joint) MRI may also be used to diagnose Management: relocation
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Liphemiarthrosis and hemarthrosis in knee
Lipohemarthrosis: Results from intra articular fracture with escape of fat and blood from bone marrow into the joint Most commonly seen in the knee and associated with tibial plateau or distal femoral fracture (rarely patellar fracture) Fatty marrow separates from water based blood and lays above it forming fat fluid level (FBI sign) which can be seen on all imaging Hemarthrosis in knee: Bleeding in the joint cavity (subtype of a joint effusion) Can occur with trauma, intra articular fracture, ACL/PCL tear, patella dislocation, meniscus tear, quad/patella tendon rupture XR shows wide overlap in XR similar to joint effusions; displaces normal structures (fat bads and bones and tendons) mimicking dislocation USS may show effusion Management consists of removal of underlying cause (correct coagulation etc) Aspiration of hemarthrosis is controversial due to infection risk In cases of haemophilia recurrent hemarthrosis can result in haemophilic arthropathy
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quadriceps and patella tendon rupture
Quadriceps tendon rupture: Eccentric loading of leg while slightly bent such as changing direction while running or landing from jump Can also occur with direct blow to knee particularly in younger patients Often hear pop or tearing sensation Inability to extend the knee against resistance or inability to straight leg raise May be preserved in partial tears Ix: XR, USS, MRI Patella tendon rupture: Very strong force needed to tear patella tendon Falls with direct impact to front of knee is common cause Cuts often associated with this type of injury Jumping can tear tendon when knee is bent and foot planted moderate sprain/strain: PRICE and HARM protocol full ruptures require surgical referral
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knee dislocations
Associated with high rate of neurovascular injuries so rapid assessment is critical Common peritoneal nerve injury (25% incidence), popliteal artery damage in 20-30%, tibial nerve injury less common Fractures are present in 60% of dislocation and ligaments at risk of injury as well as displaced menisci, patella tendon rupture etc. Present with obvious knee deformity after low/high impact trauma Risk factors are morbid obesity for lower mechanism of impact injury Hyperextension injury usually causes anterior dislocations and is most common cases Posteriorly directed force across proximal tibia (dashboard injury) causes posterior dislocations Lateral/medial dislocations often due to varus/valgus force and involve ACL and PCL tears often Rotatory action is least common causing posterolateral dislocations, usually irreducible Schenck classification categories dislocation based on pattern of multiligamentous injury Management need immediate knee reduction ideally closed procedure followed by rapid neurovascular assessment Posterolateral dislocations may need open reduction (surgery) After relocation generally follow immobilisation and conservative rehabilitation
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schenck knee dislocation classification
KD I - single cruciate and collateral injury KD II - ACL and PCL injury KD III M - ACL, PCL and MCL injury KD III L - ACL, PCL and LCL injury KD IV - ACL, PCL, MCL, LCL and posterolateral corner injury KD V - dislocation and fracture
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hip dislocation
Relatively rare and may be congenital or acquired Accounts for 5% all dislocations Numerous patterns of dislocation: posterior (most common), anterior inferior, anterior superior, central hip (protrusio) Central hip dislocation is always associated with acetabular fracture Acquired hip dislocation is normally associated with high speed trauma (motor collisions etc) and is the second most common complication of hip joint replacements (5% patients with 60% being recurrent) Congenital hip dislocation considered part of developmental dysplasia of the hip Complications include avascular necrosis particular if reduction of joint is postponed for >24 hours via occlusion of medial collateral branch which supplies the head of the femur
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ankle fractures/dislocations
Bosworth fracture: No longer used by refers to a fracture dislocation of the ankle with fracture of the fibula and posterior dislocation of the talus Pilon fracture: Distal tibial fracture involving tibial plafond (posterior malleolus) Typically from high energy injury Classified by Ruedi and allgower scale types I-III describing displacement and impaction XR and CT help determine extent of injury Trimalleolar fracture: Three part fracture of ankle Involved medial malleolus, posterior aspect of tibial plafond (posterior malleolus) and lateral malleolus Three part dislocations are unstable and may be associated with ligament injuries Measuring the size of the fracture as percentage of the total articular surface using lateral XR/CT is useful to determine if internal fixation is needed (articular steps >1mm also indication for internal fixation) Wagstaffe-Le fort fracture: Avulsion fracture of medial distal fibula due to avulsion of anterior tibiofibular ligament attachment
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pseudo gout overview
Calcium pyrophosphate deposition disease (CPDD) Form of arthritis characterised by sudden, painful swelling in one or more joints usually the knees Last for days/weeks Presents very similarly to gout, crystal deposits cause both conditions but the type of crystals vary for each The only way to differentiate from pseudogout is crystal analysis!! Gout = negatively birefringent (yellow and needle like). Pseudogout = weakly positively birefringent (blue and rhomboid shaped). Unclear why crystals forms in joints but risk increases with age Treatment helps relieve pain and reduce inflammation
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vitamin D insufficiency and risk factors
Produced naturally by diet or skin. Recommended daily intake is 400 IU (10 mcg) in the UK for adults. Over 90% is from sunlight. Food sources include oily fish, egg yolks, margarine, cereals. Insufficiency = not deficient but getting there (25-50nmol/L) Deficiency = <25nmol/L) must consider potential causes! Consider follow ups to see if responding or any other potential causes Rickets in children and osteomalacia in adults are extreme manifestations of severe vitamin D deficiency caused by inadequate mineralisation of the bone matrix (low calcium and phosphate leading to secondary hyperparathyroidism) ``` Risk factors: Dark skin especially south asian, african and middle eastern Children and those >65 YO Pregnancy Obesity Routine covering of face and body Infant exclusively breast-fed particularly after 6 months housebound/institutionalised Poverty Vegetarianism Alcoholism Living in high latitude countries Family history ```
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vitamin D deficiency presentation
``` Children: Seizures or tetany Rickets (bowing of the legs and knock knees) Anterior bowing of femur and internal ankle rotation Wrist swelling, soft deformable skull Irritable Reluctant to weight bear Impaired growth Increased infection susceptibility Cardiomyopathies including HF ``` ``` Adults: Pain and proximal muscle weakness Rib, hip, foot, thigh pain are typical Diffuse muscle aches and weakness Low bone density of DEXA scan/osteopenia Pathological fractures ```
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Vitamin D deficiency ix and Mx
Investigations: Bloods: renal function, U+Es, LFTs, parathyroid hormone, Ca and phosphate, FBC (anaemia = malabsorption) Urine microscopy - underlying CKD Serum vitamin D XR may show Champagne glass metaphyses fraying/cupping in children or looser's zone fractures and cortical bone lucency (osteomalacia) Management: Referral to paediatrician (children) and give loading dose 400IU calciferol Dietary advice, encourage safe sunlight exposure, vitamin D supplementation (calcichew) Treat underlying conditions Analgesia Orthopaedic referral if needed Most vitamin D deficiencies are treated with lifestyle changes but for those with certain conditions such as osteoporosis or Crohn's, vitamin D is treated with supplements Anyone with deficiency consider referral - screen for red flags of cancer or malabsorption Screen for hypercalcaemia, Are they dehydrated If all these options are clear then we can treat so as to make sure we are not masking any symptoms of something more sinister Monitor vitamin D, PTH and calcium every few weeks to start then 3-4 months then every 6-12 months
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reactive arthritis
Form of seronegative spondyloarthritis clinically associated with inflammatory back pain, additive or migratory oligoarthritis and extra articular symptoms that typically follow a GI or urological infection after 1-6 weeks The presence of large joint oligoarthritis, urogenital tract infection and uveitis is termed Reiter’s syndrome (clinical subtype of reactive arthritis) Strong association with HLA B27 (75% cases) and seronegative arthropathies Most commonly affected young adults with HLA B27 gene C. trachomatis and chlamydia pneumoniae are the most frequent causative pathogens May be associated with TB (Poncet’s disease) Divided into two subgroups: Postenteric: three most commonly associated enteric pathogens are Campylobacter, salmonella and shigella species Post Venereal: following chlamydia trachomatis infection or with HIV
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reactive arthritis presentation
Usually develops 2-4 weeks after GU or GI infection Onset often acute with malaise, fatigue and fever Asymmetrical predominantly lower extremity oligoarthritis Lower back pain Heel pain from achilles inflammation or plantar aponeurosis insertion Reiter’s syndrome: urethritis, conjunctivitis and arthritis Skin may show erythema nodosum or circinate balanitis Nails may show dystrophic changes Mucous membranes may show mouth ulcers Eyes: uveitis, episcleritis, keratitis, corneal ulcerations GI: abdominal pain and diarrhoea, IBD like symptoms CV: aortitis, aortic regurgitation, conduction defects
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reactive arthritis investigations
Bloods: ESR; CRP high; FBC normocytic normochromic anaemia; milk leukocytosis and thrombocytosis in acute phase HLA B27 +ve Joint aspiration to rule out septic arthritis or crystalline arthritis Stool culture, throat or urogenital tract swab/samples to identify causative organism STI screening XR ECG for conduction abnormalities
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reactive arthritis management
Acute phase: rest joint and aspirate synovial fluid Physiotherapy referral/exercises NSAID analgesia Steroids (intraarticular or oral) Antibiotics to treat underlying causative organism Usually self limiting condition within 3-12 months but can persist for longer, minority of patients may develop long term sometimes destructive arthritis, enthesitis or spondylitis High recurrence rate in those with HLA B27 gene triggered by new infection or other stress factor
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epicondylitis
Tendon overload injuries which after minor traumas lead to insertion of the extensor (tennis) or flexor (golfers) muscles of the forearm May be seen in any age group if hobbies, jobs or sports activities can lead to overuse injuries in these areas Tennis elbow peak incidence between 40-50 YO Golfers elbow is the most common cause of medial elbow pain however the incidence if about one fifth as common as tennis elbow Pathology: Thought to be a result of proliferative reaction due to chronic overload of the muscle/tendon Causes thickening of the tendon which if not treated can progress to tendon disrepair and eventual degeneration Any repetitive forceful work or leisure activity often causes tendon to swell e.g. tennis, heavy lifting jobs, awkward positions, new and unaccustomed strains like DIY, lifting new baby, moving house, carrying luggage etc. or for golfer elbow: golf or sports involving throwing or gripping, repetitive elbow movement, computer use, vibrating tools use
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tennis elbow and presentation
Reactive tendon pathology of the extensor forearm muscle common tendinous insertion causing lateral elbow and upper forearm pain and tenderness. Caused by repetitive stress at the muscle-tendon junction and its origin at the lateral epicondyle Presentation: Usually history of gradual onset Unilateral but can be bilateral - dominant arm in 75% cases Pain and tenderness over lateral epicondyle of humerus radiating to forearm and pain on resistant DORSIFLEXION of the wrist or middle finger. Tender spot usually below lateral epicondyle on outside of elbow Pain worse with use of affected muscles (opening a jar etc) and exacerbated by active resisted movements of extensor muscles of forearm Range of movement NOT restricted Mill’s test: straighten arm and palpate lateral epicondyle, fully flex wrist, pronate forearm (painful = +ve) Cozen’s test: elbow flexed, makes fist and deviates wrist radially with forearm pronated. Resisted extension of wrist (+ve pain in lateral epicondyle)
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golfers elbow and presentation
Reactive tendon pathology of flexor forearm muscles, causing medial elbow pain. Caused by repetitive stress at the muscle tendon junction and its origin at the medial epicondyle Presentation: Pain and tenderness maximal over medial epicondyle, radiating into forearm Aggravated by wrist flexion and pronation Dull ache at medial epicondyle Onset of pain usually gradual and aggravated by using affected muscles (grasping objects or shaking hands) Golfer’s elbow test: pronate and flex the wrist and forearm at the same time (turn palm up to palm down and bends wrist back towards them) +ve if pain in medial epicondyle Associated neuropathy may cause decreased sensation or paraesthesia in 4/5th fingers or muscle weakness if severe
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management of epicondylitis (tennis and golfers elbow)
NSAIDs and PPI until inflammation and symptoms resolve PRICE - rest for week or so, slow return to movements but avoid strenuous or triggering movements (i.e. whatever set it off in the first place) Referral to physiotherapy Steroid injections Acupuncture Orthotics - splints, casts, straps or braces to help support muscles
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adhesive capsulitis/frozen shoulder
One of the most common causes of intrinsic shoulder pain Glenohumeral disorder and can occur in one shoulder or both at once Thickening and contraction of the glenohumeral joint capsule and formation of adhesions cause pain and loss of movement Can occur spontaneously, following rotator cuff lesions/injury or in mobility conditions eg after a stroke or plaster immobilisation Most commonly affects ages 40-65 and is more common in women 2-4 x higher incidence in diabetes and also associated with thyroid disease Phases: Severe generalised pain associated with stiffness. Daily activities limited and can last up to 9 months Pain usually gradually subsides but the shoulder remains stiff. Movement can become more limited, especially external rotation. Can last between 4-12 months Shoulder becomes less stiff and there is an increase in ROM usually lasting 1-3 years
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frozen shoulder presentation and investigations
Presentation: Pain usually followed by stiffness in the shoulder Usually affects the non-dominant shoulder Gradual severe pain onset associated with stiffness Restricted active and passive movement of whole shoulder Inability to sleep on affected side Restricted activity Investigations: Clinical diagnosis: whole shoulder tender to palpation and limited active and passive ROM especially external rotation (elbow to side and move arm out as far as they can) XR for atypical presentation or non-responsive to treatment but are commonly normal Bloods if red flags present
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frozen shoulder management, prevention, complications and prognosis
Management: Simple analgesia (NSAID and paracetamol) Physiotherapy and stretching exercises Passive mobilisation Steroid injections for symptoms or oral steroids for short term relief Surgery (MUA) to passively move thickened inflamed ligaments and stretch capsule Referral to secondary care if significant disability >6 months despite management Complications: Long term stiffness Prognosis: Symptoms can last up to 3 years however 90% patients with spontaneous frozen shoulder recover to normal functional levels by two years without any treatment Prevention: Avoid prolonged immobilisation
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carpal tunnel syndrome
Caused by compression or irritation of the median nerve within the carpal tunnel Anything causing reduction in volume or increase in pressure within compartment can cause Incidence peaks in 50s and 70s Mostly in women (earlier age) Evidence of genetic component although exact mechanism is unknown Main risk factor is occupational - dentists and shipyard workers using high powered vibrating tools Carpal tunnel in an anatomical compartment of the hand; bound by three sides of carpal bone and transverse carpal ligament (flexor retinaculum) Contains 9 tendons and 1 nerve: median nerve, four tendons of flexor digitorum superficialis, four of flexor digitorum profundus and flexor pollicis longus
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carpal tunnel syndrome associations
``` Most cases are idiopathic but may be associated with: Pregnancy Overuse Trauma Obesity Renal failure Diabetes Inflammatory arthropathy Post-Colles fracture flexion/extension injury Use of walking aids Conditions encroaching on space within carpal tunnel (aneurysm, neurofibroma, haemangioma, lipoma, ganglion, xanthoma and gouty tophi) Menopause Inflammatory arthritides of wrist Acromegaly Renal dialysis Amyloidosis ```
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carpal tunnel syndrome presentation
Tingling Numbness Pain in median nerve distribution can become more persistent, radiating to forearm, elbow, arm or shoulder (thumb, index and middle finger) Often worse at night causing wakening Weakness in hand grip and opposition of thumb Muscle wasting in thenar compartment in severe cases Can be bilateral although may not be present at the same time
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investigations for carpal tunnel
Phalen's maneuver: raise arms shoulder level, bring dorsum of hands together in midline, hold wrist in flexed position for 30-60 seconds - +ve test causes tingling and numbness over median distribution Tinel test: tapping lightly over median nerve at wrist causes distal paraesthesia in median nerve distribution Compression test: pressure over proximal carpal tunnel (wrist crease) with thumbs causes paraesthesia in median nerve distribution Diagnostic doubt: electroneurography is GOLD STANDARD Electromyography USS MRI
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management for carpal tunnel and prognosis
Conservative: For mild or early disease or minimal symptoms Symptoms may resolve within 6 months (most likely in young people <30) if symptoms are unilateral and short duration or in women who fluid retention in pregnancy is main cause Splints beneficial to sleep in Minimise exacerbating activities Steroid injections - also used for diagnostic Physiotherapy and stretching Surgical: Patients with severe symptoms, motor weakness of thumb or persistent sensory or motor disturbance then surgery for decompression can be done Can produce surgery related pain, hand weakness and complications from surgery Prognosis: Symptoms can resolve within 6 months in about ⅓ patients particularly younger patients Poor prognosis often associated with bilateral symptoms and positive phalen test However the severity of symptoms often doesn’t correlate will with extent of nerve compression
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kyphosis/scoliosis
Spinal deformities rarely occur in single plane and usually in 3D Combined kyphosis and scoliosis is called kyphoscoliosis In early childhood around 60% are boy but in adolescence is around 90% Screening should be directed at girls at maximum age of incidence and boys should be screened at a slightly later age but girls:boys ratio is 9:1 Scoliosis is much more common to the RIGHT except in infantile type where left sided is more common Infantile scoliosis occurs before age 3 and is more common in boys. Many cases resolve spontaneously Juvenile scoliosis is found more frequently in girls between ages 3-10 and curves has a high risk for progression and often need surgical intervention Adult scoliosis occurs after maturity Kyphosis: excessive curvature of the spine in the sagittal AP plane. Normal back has 20-45 degrees of curvature in the upper back and anything >45 degrees Scoliosis: abnormal curvature of the spine in the coronal lateral plane. Between 10-20 degrees is mild. Less than 10 degree in postural variation Lordosis: or hyperlordosis is excessive curving of the lower spine and is often associated with scoliosis or kyphosis. Can be exaggerated by poor posture
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types of scoliosis and risk factors
Types of scoliosis: Idiopathic (80%) Congenital malformation of vertebrae 10% Neuromuscular conditions (cerebral palsy, spina bifida and poliomyelitis) Crush fracture Metabolic problems like Hunter’s syndrome Dysmorphic syndromes such as neurofibromatosis, marfan’s syndrome, osteogenesis imperfecta Risk factors: Spinal column disease/trauma Osteoporosis family history
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scoliosis presentation and investigations
Mild disease usually painless but pain increases with increasing deformity Unlevel shoulders, waistline asymmetry or rib prominence Adams forward bend test: ask the patient to bend forward and note if curvature increases or lessens with this maneuver. Fixed scoliosis becomes more obvious on flexion. If there is mild scoliosis try placing a wedge under one foot and note if this improves the condition, if it worsens then try the other leg Investigations: Clinical diagnosis Adams forward bend test Scoliometer to measure curve rotation PA and lateral XR of spine (Cobb’s angle to measure degree of scoliosis) Radionucleotide bone scan Oxygen sats and FVC in more severe deformity
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management of scoliosis
Early diagnosis and intervention is beneficial, consists of observation, orthosis and operation Infantile idiopathic scoliosis has the best prognosis and recovery at 90% but double curves have worse prognosis. Braces and casts can be worn or surgery needed if curvature is too severe Juvenile idiopathic scoliosis is considered the most severe type, approximately 70% patients will ultimately need surgery Adolescent idiopathic scoliosis is the most common type. Small curves have low progression risk so can be monitored conservatively, larger curves in immature patients have higher risk at 70%. Bracing or surgery needed for rapid change in curvature Physiotherapy exercises to compensate and self correct deformities Surgery is recommended for those with Cobb’s angle >45-50 degrees
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kyphosis management
Postural round back is thoracic kyphosis while standing, does not progress and resolves spontaneously Scheuermann’s disease produces thoracic kyphosis >40 degrees with true structural changes within thoracic vertebrae with 5 degrees of wedging in each of three adjacent vertebrae measured on side view films. Usually painless. Observation enough for <60 degree angles, brace treatment for curves between 60-80 but surgery rarely needed. Subtype of Scheuermann’s is in the lumbar spine usually in men with heavy lifting jobs. Changes in the vertebrae and disc reflect physical stress effects. Treatment is to stop the offending activity.
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scoliosis/kyphosis complications and prognosis
Respiratory muscle weakness and reduced exercise capacity Distortion of spinal column may cause restriction of the chest with impaired lung function Abdominal contents compression Severe deformity may impinge on the spinal cord and cause paraplegia May be associated with psychological problems especially in adolescents Prognosis: The younger the child and the greater the curvature the worse the prognosis
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de Quervain's tenosynovitis and risk factors
Painful condition affecting the tendons on the thumb side of the wrist Hurts to turn wrist, grasp or make a fist, repetitive hand movements Exact cause is unknown but thought to be from direct injury and scar tissue restricts tendon movements or inflammatory arthritis ``` Risk factors: Ages 30-50 Female Pregnancy Repetitive hand and wrist motions (jobs/hobbies) ```
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de Quervain's tenosynovitis presentation, complications and investigations
Pain at base of thumb Swelling at base of thumb Difficulty moving thumb and wrist when grasping or pinching sticking/stop and go sensation when moving the thumb If untreated can radiate into forearm aggravated by pinching, gripping movements Complications: Loss of function or range of motion in wrist and hand Investigations: Clinical diagnosis Finkelstein test: bend thumb across palm of hand and bend fingers over the thumb. Bend wrist toward little finger. If this causes pain on the thumb side then +ve test for de Quervain’s tenosynovitis
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de Quervain's tenosynovitis management
Started early symptoms should resolve in around 4-6 weeks. If symptoms started in pregnancy they’re likely to end around end of pregnancy or during breastfeeding NSAIDs Steroid injections Splint or brace Avoid repetitive movements and apply ice as needed Surgery to open sheath and free up tendons if severe
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trigger finger
Aka stenosing tenosynovitis Painful condition affecting one or more of the hands tendons making it difficult to bend the affected finger/thumb Caused by tendon sheath inflammation and swelling meaning the tendon can no longer easily slide through the sheath and can bunch up forming nodules making movement difficult Tendon can become swollen and inflamed and can catch in the tendon sheath making movements on the fingers difficult or giving a clicking sensation Usually affected the thumb, ring finger or little finger More common in dominant hand (mostly right hand) Exact cause is unknown but more common in women >40 YO and can be associated with Dupuytren's contracture, diabetes and RA Trigger finger in children is less common but can present in those aged 6 months - 3 years. It is rarely painful and usually gets better without treatment
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trigger finger presentation and management
Pain at base of affected finger/thumb with palpation Stiffness or clicking with movement particularly worse in the morning Fingers may get stuck in bent position then suddenly pop straight Eventually may not be able to straighten at all Management: May resolve without treatment however if not treated may become permanently deformed/bent Rest from triggering activities NSAIDs for pain Steroid injections to reduce swelling Surgery to relieve pressure of tendon sheath only when all other treatment fails
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rotator cuff disorders overview
Term subacromial pain/impingement/rotator cuff syndrome/painful arc syndrome refers to all rotator cuff lesions including tendon disease Pathology in ages 35-75 usually result from tears in rotator cuff muscles Cause can be from degeneration (most commonly) or sudden injury/fall Most often presents in patients aged 35-75 YO Subacromial impingement is the most common cause of shoulder pain May be caused by repetitive movements or heavy lifting especially above shoulder level, however often occur in non-dominant arm in non-manual workers May show muscle wasting with pain on movements and partial restricted active movement (passive is full range but painful) Painful arc between 70-120 degrees of active abduction increases likelihood of RCD Rotator cuff tear: Usually following trauma in young people but atraumatic in elderly from bony spurs on acromion undersurface or intrinsic cuff degeneration Partial tears difficult to differentiate from rotator cuff tendinopathy Drop arm test can be used to detect massive tear: passively abduct arm as high as they can then ask them to slowly lower - +ve massive tear if the arm suddenly drops <90 degrees as supraspinatus takes over Calcific tendonitis: Crystalline calcium phosphate deposited in rotator cuff tendon Cause unknown but more common in women and those aged 30-60 Self limiting condition as calcium will eventually be reabsorbed but can take many years Special tests: Assess active and passive range of movement and resisted in both shoulders Painful arc between 70-120 degrees abduction Test passive external rotation (reduced in frozen shoulder) Perform drop arm test for supraspinatus/rotator cuff massive tear Cross arm test: isolates acromioclavicular joint. Ask the patient to raise the arm to 90 degree straight in front of them then ask to adduct the arm across the chest. This will cause pain in acromioclavicular problems
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rotator cuff disorders red flags and investigations
Weight loss, deformity, mass or swelling, abdominal discomfort/swelling Overlying skin erythema (tumour/infection) Systemic illness signs or GCA/polymyalgia rheumatica signs Fever (infection/malignancy) Trauma or recent convulsion or electric shock (unreduced dislocation) Change in shoulder contour with loss of rotation(dislocation) Presence of sensory/motor deficit suggests neurological lesions ``` Investigations: Bloods: FBC, ESR, CRP and XR if red flags present USS preferred Ix for shoulder MRI for shoulder instability Spinal XR for referred neck pain ```
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rotator cuff disorders management
PRICE Rest, Ice, Compression, Elevation NSAIDs analgesia Physiotherapy exercises/referral Steroid injections if limited function due to pain (do NOT give if they have received another steroid injection with minimal/no benefit, have already had 3+ injections in the same shoulder in the last year, suspected rotator cuff tear or any CI like infection, osteomyelitis etc) Rotator cuff tears may need orthopaedic referral if severe for arthroscopic tendon repair Acromioclavicular disease - PRICE and consider sling for 5-7 days if injury suspected)
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rheumatoid arthritis
Autoimmune condition causing chronic inflammation of the synovial lining of the joints (synovitis), tendon sheaths and bursa It is an inflammatory arthritis Tends to be symmetrical affecting multiple joints (symmetrical polyarthritis) Inflammation of the tendons increase risk of tendon rupture 3:1 F:M ratio Often develops in middle age but can be at any age Family history increases risk of RA Associated with HLA DR4 (often +ve in RF +ve patient) and DR1 (occasionally present in RA patients) genes Rheumatoid factor is an autoantibody presenting in around 70% of RA patients. It targets IgG antibodies causing autoimmune destruction (usually an IgM but can be any class Ig) Cyclic citrullinated peptide antibodies (Anti-CCP antibodies) are autoantibodies that are more sensitive and specific to RA than RF. anti-CCP antibodies often pre-date development of RA and give an indication that the patient will go on to develop it at some point 75% patients develop joint pain, swelling and flares, 5% develop severe disease and 20% always have mild disease
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rheumatoid arthritis presentation
Symmetrical distal polyarthropathy Pain Swelling Stiffness of joints affected Typically in small joints of hands and feet and wrists, ankle Can also present in larger joints (knees, shoulders, elbows) Onset can be very rapid (overnight) or over months/years Fatigue Weight loss Malaise Muscle aches and weakness Pain is worse at rest and improves with activity (early morning stiffness is key symptom) hands: Palpation of synovium in joints will give a boggy feeling from inflammation and swelling Z shaped deformity to thumb Swan neck deformity (hyperextended PIP with flexed DIP) Boutonnieres deformity (hyperextended DIP with flexed PIP) - due to tear in central slip of the extensor component of fingers. This means when trying to extend the finger the flexor digitorum superficialis tendons pull on the distal phalanx without any other supporting structure causing DIPs to extend and flex the PIPs Ulnar deviation of fingers at knuckle (MCP) Extra-articular manifestations: Pulmonary fibrosis with nodules (Caplan’s syndrome) Brochiolitis obliterans (inflammation causing small airway destruction) Felty’s syndrome (RA, neutropenia and splenomegaly) Secondary Sjogren’s syndrome (aka sicca syndrome) Anaemia of chronic disease Cardiovascular disease Episcleritis and scleritis Rheumatoid nodules Lymphadenopathy Carpal tunnel syndrome Amyloidosis
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palindromic rheumatism
Self limiting short episodes of inflammatory arthritis with joint pain, stiffness and swelling typically affecting only a few joints. Episodes last only 1-2 days with complete resolution after Having positive antibodies (RF and anti-CCP) may indicate it may progress to RA eventually Commonly affects PIP, MCP, wrist and ankle joints, cervical spine and knees, hips and shoulders can also be affected (IP joints almost never affected in RA so if IP joints are painful it is most likely osteoarthritis!!)
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atlantoaxial subluxation
Occurs in the cervical spine Axis and odontoid peg shaft within the atlas Caused by local synovitis and damage to ligaments and bursa around the odontoid peg of the axis and atlas. Can cause spinal cord compression and is a medical emergency Particularly important if the patient is having general anaesthetic and needing intubation MRI can visualise changes in these areas as part of pre-op assessment
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rheumatoid arthritis investigations and diagnosis
Clinical diagnoses Bloods: Rheumatoid factor and anti-CCP antibodies; CRP and ESR; FBC (WCC) XR of hands and feet may show joint destruction and deformity, soft tissue swelling, osteopenia, bony erosions USS to evaluate and confirm synovitis - particularly useful when clinical findings are unclear Measure functional ability using HAQ to assess for baseline for response to treatment American college of rheumatology (ACR)/european league against rheumatism (ELAR) from 2010 criteria: Joints involved (more and smaller joints = higher score) Serology (RF, anti-CCP) Inflammatory markers (ESR; CRP) Duration of symptoms (more/less than 6 weeks) Score of >6 indicates diagnosis Disease activity score (DAS28): Based on assessment for 28 joints and points are given for swollen joints, tender joints and ESR/CRP results Useful in monitoring disease activity and response to treatment
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management of rheumatoid arthritis
Measure functional ability using HAQ to assess for baseline for response to treatment Early treatment gives better outcomes, essential to use MDT (specialist nurses, physio, occupational therapy, psychology and podiatry) Short course steroids for first presentation and flare ups NSAID/COX-2 inhibitors effective for pain relief along with PPI gut protection: Paracetamol, codeine (30-60mg QDS), tramadol (50-100mg QDS up to 4x more effective with paracetamol) are very effective most cases respond to first line NSAID they’re given Amitriptyline up to 150mg daily if needed adjuvant to simple analgesia COX-2 inhibitors like celecoxib and etoricoxib (don’t need to prescribe PPI longside as gut risk not hight) Monitor CRP/HAQ/DAS28 to evaluate treatment response and monitor condition and try to achieve minimal effective dose with each patient Disease modifying anti-rheumatic drugs (DMARDs): Start within 3 months of diagnosis to minimise joint damage First line monotherapy with methotrexate (15mg weekly injection), leflunomide or sulfasalazine (hydroxychloroquine considered in mild disease as is mildest rheumatic drug) must co-prescribe folic acid Second line to use combination of above Third line methotrexate plus biological agent (TNF inhibitor e.g. adalimumab, infliximab and etanercept) Biological agents: Fourth line is rituximab Pregnant women tend to improve symptoms during pregnancy due to natural increase in steroid hormone production Surgery for joint replacement if joint deteriorates beyond medical relief
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key considerations for rheumatoid arthritis management
Counsel before starting on monotherapy (increased risk of bruising/bleeding and then specifics of each drug) Emphasise dose and provide leaflets and details Monitoring: all DMARDs should have baseline height, weight and BP measured, FBC, renal profile, serum albumin, LFTs, serum PIINP in those with psoriasis Screening for HIV, HBV and HCV recommended as well as VZV FBC, renal and LFTs every 1-2 weeks until stabilised therapy then at least 6 weeks then 3 months may be more frequent in high risk patients same with every change of dose. If methotrexate combined with leflunomide then continue monthly monitoring until stable for 12 months then consider reducing on individual basis U+Es every 1-2 weeks for first month until steady dose
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DMARD and biological agent side effect overview
Methotrexate: pulmonary fibrosis Leflunomide: Hypertension and peripheral neuropathy Sulfasalazine: Male infertility (reduces sperm count) Hydroxychloroquine: Nightmares and reduced visual acuity Anti-TNF medications: Reactivation of TB or hepatitis B Rituximab: Night sweats and thrombocytopenia
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Sjogren's syndrome overview
Autoimmune condition that affects the exocrine glands Leads to symptoms of dry mucous membranes (dry mouth, dry eyes and dry vagina) Primary is where condition occurs in isolation Secondary occurs related to SLE or rheumatoid arthritis Associated with anti-Ro and anti-La antibodies Schimer test involved inserting folded pieces of filter paper under the lower eyelid with a strop hanging out over the eyelid. Left in for five minutes and the distance along the strip hanging out becomes moist and this is measured. Tears should usually travel 15 mm in healthy young adults. A result of <10mm is significant Management involves artificial tears, artificial saliva, vaginal lubricants and hydroxychloroquine to halt progression of the disease Complications include eye infection (conjunctivitis and corneal ulcers, oral problems such as dental cavities and candida infections, vaginal problems such as candidiasis and sexual dysfunction Can rarely affect other organs causing complications like pneumonia and bronchiectasis, non-Hodgkin's lymphoma, peripheral neuropathy, vasculitis and renal impairment
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polymyositis overviel
Autoimmune disorder where there is chronic inflammation of the muscles Dermatomyositis is a connective tissue disorders with chronic inflammation of skin and muscles Presents with muscle pain, fatigue and weakness, occurs bilaterally and typically affects proximal muscles Mostly affects the shoulder and pelvic girdle and develops over weeks Polymyositis occurs without any skin features, while dermatomyositis is associated with skin involvement (Gottron lesions, photosensitive erythematous rash, purple rash on face and eyelids, periorbital oedema, subcutaneous calcinosis) Autoantibodies associated with polymyositis are anti-Jo-1 and those associated with dermatomyositis are anti-M-2 and ANAs Diagnosis based on clinical presentation, elevated creatine kinase, autoantibodies present and EMG studies as well as muscle biopsy to establish diagnosis Management guided by rheumatologist. May need physiotherapy, screen for underlying cancers, occupational therapy Corticosteroids first line treatment Immunosuppressants (azathioprine), IV Igs and biological agents (infliximab or etanercept) are used when steroids are not effective
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systemic lupus erythematosus
Inflammatory autoimmune connective tissue disease Affects multiple organs and causes typical red malar rash across the face Presents with varying and non-specific symptoms More common in women and Asian’s and usually presents in young-middle aged adults but can present in later life Often takes a relapsing-remitting course with flares and periods where symptoms are improved Result of chronic inflammation means patients with lupus often have shortened life expectancy Cardiovascular disease and infection are leading causes of death Pathophysiology: Characterised by antinuclear antibodies These are antibodies to proteins within the cell nucleus causing the immune system to target these proteins Generates inflammatory response in the cell causing the presenting symptoms
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SLE presentation and complications
``` Fatigue Weight loss Arthralgia and non-erosive arthritis Myalgia Fever Photosensitive malar rash (butterfly rash on nose and cheeks) that gets WORSE IN SUNLIGHT LAP and splenomegaly SOB Pleuritic chest pain Mouth ulcers Hair loss Raynaud’s phenomenon: ``` ``` Complications: CVD Infection Anaemia of chronic disease (chronic normocytic anaemia, leucopenia, neutropenia, thrombocytopenia) Pericarditis Pleuritis/pleurisy Interstitial lung disease Neuropsychiatric SLE (optic neuritis, transverse myelitis) Recurrent miscarriage Venous thromboembolism ```
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SLE Ix and Mx
Investigations: Autoantibodies (ANA, anti-dsNDA, anti-Smith, APS antibodies) SLICC or ACR criteria for diagnosis: confirm antibody presence and number of clinical features suggestive of SLE management: Anti-inflammatory and immunosuppressive medications First line NSAIDs, steroids (prednisolone), hydroxychloroquine (first line for mild SLE), sun cream and sun avoidance with malar rash Methotrexate, mycophenolate mofetil, azathioprine, tacrolimus, leflunomide, ciclosporin Biological therapies: rituximab
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scleroderma/systemic sclerosis
Often used interchangeably, most patients with scleroderma have systemic sclerosis However there is a localised scleroderma that only affects the skin Scleroderma = hardening of the skin Systemic sclerosis is an autoimmune inflammatory and fibrotic connective tissue disease Cause is unclear Affects the skin in all areas as well as internal organs Two main disease patterns: Limited cutaneous systemic sclerosis Diffuse cutaneous systemic sclerosis
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limited vs diffuse cutaneous systemic sclerosis/scleroderma
``` Limited: CREST syndrome Calcinosis Raynaud’s phenomenon Esophageal dysmotility Sclerodactyly Telangiectasia ``` Diffuse: includes CREST syndrome features as well as internal organs causing: CVD (HTN and CAD) Lung problems: pulmonary HTN and fibrosis Kidney problems: glomerulonephritis and scleroderma renal crisis
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scleroderma presentation
Hardening of the skin giving shiny, tight skin appearance without creases or folds, most noticeable on hands and face Sclerodacytly - as skin tightens around the joints it restricts range of motion and reduces function as well as loss of fat pads on fingers. Skin can break and ulcerate Telangiectasia Calcinosis: calcium deposits under the skin, most commonly fingertips Rayneud’s phenomenon: fingertips go completely white then blue in response to mild cold. Caused by vasoconstriction of vessels and commonly occurs without sclerosis however is classical feature of disease Esophageal dysmotility caused by connective tissue dysfunction commonly causes swallowing difficulties, acid reflux and oesophagitis Systemic and pulmonary HTN caused by connective tissue dysfunction in systemic and pulmonary arterial systems. Can be worsened by renal impairment Pulmonary fibrosis in severe disease Scleroderma renal crisis: acute condition with severe HTN and renal failure
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scleroderma Ix and Mx
Investigation: Autoantibodies: ANA, anti-centromere (associated with limited form), anti-scl-70 (associated with diffuse form and more severe disease) Nail fold capillaroscopy: magnify and examine nailfold look for abnormal capillaries Diagnosis based on ACR and EULAR criteria involving clinical features, antibodies and nailfold capillaroscopy results Management: Specialist MDT Steroids and immunosuppressants with diffuse disease and complications like pulmonary fibrosis Smoking cessation, gentle skin stretching exercises, regular emollients, avoid cold triggers, physiotherapy, occupational therapy Nifedipine for Raynaud’s phenomenon PPIs and promotility agents for GI symptoms Antibiotics for skin infections Antihypertensives (ACEi usually) Pulmonary HTN management Supportive management of pulmonary fibrosis
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juvenile rheumatoid/idiopathic arthritis
Refers to condition affecting children and adolescents where autoimmune inflammation occurs in the joints Diagnosed where there is arthritis without any other cause lasting >6 weeks in patient under the age of 16 Key features are joint pain, swelling and stiffness ``` Subtypes: Systemic Polyarticular Oligoarticular Enthesisits related Juvenile psoriatic ```
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systemic JIA
AKA still’s disease Systemic illness that can occur throughout childhood Typical features are subtle salmon pink rash, high swinging fevers, enlarged lymph nodes, weight loss, joint inflammation and pain, splenomegaly, muscle pain, pleurisy and pericarditis Antinuclear antibodies and RFs typically negative but inflammatory markers CRP, ESR, platelets and serum ferritin are raised Key complication is macrophage activation syndrome with severe immune system activation and massive inflammatory response. Acutely unwell child with disseminated intravascular coagulation, anaemia, thrombocytopenia, bleeding and non-blanching rash. Life threatening emergency - key investigation is finding low ESR
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polyarticular/oligoarticular JIA
In 5 joints or more Tends to be symmetrical and can affect small joints of hands and feet as well as large joints Minimal systemic symptoms (mild fever, anaemia, reduced growth) RF -ve usually described as seronegative; seropositive patients tend to be older children/adolescents and disease more similar to rheumatoid arthritis in adults oligoarticular: Involves 4 joints or less Usually only affects single joint (monoarthritis) Tends to be larger joints and more common in girls under age 6 Classic feature is anterior uveitis (must be referred to ophthalmologist) Tend not to have systemic symptoms and inflammatory markers are normal/mild ANAs often positive but RF usually negative
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enthesitis related arthritis
More common in male children over age 6 Thought of as a paediatric version of seronegative spondyloarthropathy conditions ( ankylosing spondylitis, psoriatic arthritis, reactive arthritis and inflammatory bowel disease-related arthritis. Patients have inflammatory arthritis in the joints as well as enthesitis) MRI can demonstrate enthesitis but cannot distinguish cause (stress or autoimmune) Majority of patients are HLA B27 positive Prone to anterior uveitis and should be referred to ophthalmologist even if asymptomatic Tender to localised palpation of entheses: commonly in IP, wrist, greater trochanter, quad insertion at ASIS, quad/patella tendon, achilles, MCP areas
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juvenile psoriatic arthritis
Seronegative arthritis associated with psoriasis Pattern of joint involvement varies but associated with several skin signs: psoriasis, nail pitting, onycholysis (separation of nail from bed), dactylitis, enthesitis
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juvenile idiopathic arthritis management and differentials
``` Paediatric rheumatology referral and MDT NSAIDs Steroids (oral, IM, intra articular) DMARDs (methotrexate) TNF inhibitors (etanercept, infliximab) ``` In children that have fevers for more than 5 days, the key non-infective differentials to remember are Kawasaki disease, Still’s disease, rheumatic fever and leukaemia.
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Polyarteritis nodosa
Necrotising arteritis of medium or small arteries without glomerulonephritis or vasculitis in arterioles, capillaries or venules and not associated with antineutrophil cytoplasmic antibodies (ANCAs) Can affect any organ but for unknown reasons spares the pulmonary and glomerular arteries Incidence is higher in hepatitis B endemics Mostly idiopathic but can be triggered by viral infection Peak incidence at 10YO or between 40-50 YO Men more commonly affected in adulthood but children equally affected
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Polyarteritis Nodosa presentation and investigations
Often presents with nonspecific symptoms including fever, weight loss, headache, myalgia with spectrum of organ involvement Peripheral nerves and skin most commonly affected; lesions, purpura, livedoid subcutaneous nodules, necrotic ulcers Mononeuritis GI, kidneys, heart and CNS associated with higher mortality AKI, HTN Investigations: Hep B screening FBC - leukocytosis Hypergammaglobulinemia Small artery biopsies shows necrotising inflammation Arteriography shows microaneurysms in small and medium sized vessels
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polyarertitis nodosa management
Steroid therapy If still relapse then cyclophosphamide may help reduce relapses Azathioprine maintenance therapy Management of hepatitis B infection IV Igs and aspirin effective in childhood disease
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lower back pain
Lumbosacral area of the back Affects around ⅓ adults each month In most people it is non-specific (serious specific causes are rare) Non-specific lower back pain if often a chronic problem in which periods of little pain or disability are interrupted by acute episodes of severe pain Pain often varies with posture and exacerbated by movement Very important to exclude: serious spinal pathology, inflammatory features ad sciatica ``` Complications: Chronic back pain Depression Disability Loss of employment ``` Indications: Mechanical: varies with posture, exacerbated by movement, arises from spinal joints, vertebrae or soft tissues (spasm), IVD prolapse Inflammatory: pain and stiffness on waking and is improved by movement. Caused by rheumatoid conditions (ankylosing spondylitis) Acute: present for less than 6 weeks, could be insidious required urgent medical intervention like cauda equina Chronic: present for more than 6 weeks, major cause of physical, psychological and social disability
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straight leg raise/lasegue test and Barggard sign
Patient lying supine Keep knee fully extended Flex hip and observe for pain Positive for sciatica if pain is reproduced <60 degrees Barggard sign: lower straight leg to point without pain and passively dorsiflex the foot positive if this also recreates pain
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lower back pain red flags
Cauda equina: severe/progressive bilateral neuro deficit of legs (motor weakness with knee extension etc), recent onset urinary retention/incontinence, faecal incontinence, perianal or perineal sensory loss (saddle paraesthesia), unexpected laxity of anal sphincter Spinal fracture: sudden onset central spinal pain relieved by lying down, history of trauma, structural deformity of spine, tenderness of vertebral body Cancer: 50< YO or <20 YO, gradual onset, severe unremitting pain remaining when supine, night pain, disturbing sleep, aggravated by straining, thoracic pain, spinal tenderness (localised), no improvement with 4-6 weeks conservative management, weight loss and past history of cancer Infection: fever, TB or recent UTI, diabetes, history of IV drug use, HIV infection, immunosuppressants (steroids)
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management of lower back pain
Assessing risk of back pain disability (STarT Back - score of <3 = low risk of chronicity; 4+ and subscore of 3> medium risk of chronicity; 4+ and subscore of 4+ high risk chronicity) https://startback.hfac.keele.ac.uk/training/resources/startback-online/ Simple analgesia first line (NSAID, codeine/co codamol) Short course benzodiazepines for back spasming (diazepam) Education and self help measures: staying active resuming normal activities and returning to work ASAP High risk of back disability or symptoms are not improving refer to group exercise/CBT/physiotherapy Refer to neurosurgery or orthopaedic surgeon if red flags, persistent or severe neurological deficit
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IVD prolapse
Slipped/herniated or prolapsed disc often causes severe sudden lower back pain Disc often presses on nerve root causing pain and other symptoms in a leg In most cases symptoms ease off gradually over several weeks Can occur in any vertebrae however the most common are L4/5/S1 (lumbar spine) As a rule, the larger the prolapse the more severe the symptoms are likely to be Unknown exact cause thought to be developed weakness in outer disc Pathology: Part of softer middle disc (nucleus pulposus) bulges through fibrous outer ring It may press on nerve as it leaves the spinal cord resulting in presenting symptoms of pain Some inflammation may develop around the herniated part which can also irritate the nerve and cause swelling putting additional pressure on the nerve
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IVD prolapse risk factors and presentation
``` Risk factors: 30-50 YO Male (2:1) Jobs involving lifting or lots of sitting (driving especially) Weight bearing sports Smoking Obesity Increasing age ``` Presentation: Severe usually sudden onset lower back pain Eased by lying down Worse with sneezing, coughing or moving Sciatica or other nerve root pain Paraesthesia Numbness or weakness in buttock/leg or foot Cauda equina (rare but emergency) problems with bowel and bladder (incontinence or retention), saddle anaesthesia, weakness in one/both legs Can be asymptomatic if no nerve irritation or pressure
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IVD prolapse investigation and management
Clinical diagnosis RULE OUT RED FLAGS OF CE XR MRI is best to diagnose prolapse disc Management: Conservative management for 6-8 weeks; then refer to orthopaedic or neurosurgeon if no improvement after 8 weeks Advice to carry on as normal as much as is possible to improve recovery rate Strengthening spine exercises Physiotherapy Chiropractor or osteopath for manipulation (debatable effectiveness) Analgesia until symptoms resolve (NSAIDs, codeine, amitriptyline for neuropathic pain if pain more than few days) Epidural steroid injections can be used for flares Surgery considered if >6 weeks, symptoms not improving (9/10 patients have resolved by 6 weeks) Prevention: Regular activity and exercise (running, swimming etc) Back safety awareness - manual handling
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cauda equina
Spinal emergency Disease affecting the tail end of the spinal cord (cauda equina) Cauda equina is formed by nerve roots in caudal to level spinal cord termination The syndrome is caused by compression of the nerves causing bladder/bowel dysfunction, reduced sensation in saddle area and sexual dysfunction with possible neurological deficit in lower limb ``` Causes: Herniation of lumbar disc is most common cause Tumours Trauma Infection including epidural abscess Congenital Spongylolithesis Postoperative haematoma After spinal manipulation Sarcoidosis ```
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cauda equina presentation
Most cases have sudden onset and progress rapidly within hours or days but can evolve slowly and patients do not always have pain Low back pain with pain in legs (uni or bilateral) motor/sensory abnormality Lower limb weakness bowel/bladder dysfunction with saddle anaesthesia Urinary retention/incontinence, bowel incontinence/constipation Sexual dysfunction
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cauda equina Ix and Mx and complications
``` Investigations: Clinical diagnosis MRI Myelography or CT Urodynamic studies ``` Management: Immobilise spine if trauma Surgery to remove blood, bone, tumours, herniated discs or growths Lesion debulking for space occupying lesions (tumours/abscesses) Radiotherapy is malignant NSAIDs if ankylosing spondylitis Infection treated Address lifestyle issues, physiotherapy PRN Complications: Paralysis Sensory abnormalities bladder/bowel and sexual dysfunctions
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spinal stenosis
Caused by narrowing of the spinal canal or neural foramina producing root ischaemia and neurogenic claudication Most often caused by loss of disc space, osteophytes and hypertrophic ligamentum flavum Not all patients with narrowing develop symptoms however it can progress causing compression of spinal nerves or spinal cord compression Most often affected the kumbar/cervical spine Symptomatic stenosis of thoracic spine is very uncommon Lateral recess stenosis tends to cause sciatica Central spinal stenosis tends to cause spinal claudication (neurogenic claudication: bilateral calf pain, paraesthesia or numbness on walking)
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cervical and lumbar spinal stenosis
cervical Occurs in 9% people over 70 usually in the lower cervical segments Most characteristic symptoms are neck pain with restricted movement of neck, instability of gait, loss of fine motor control of upper limbs, weakness and sensory disturbance in upper and lower limbs and urinary urge incontinence +ve Babinski sign Conservative management: physiotherapy, epidural injections and NSAIDs and other analgesia Surgical options include anterior discectomy and fusion, anterior corpectomy and fusion, arthroplasty (highly select cases), posterior laminectomy +/- fusion or laminoplasty Lumbar spinal stenosis: Thought to occur in roughly 10% of the population but true incidence is higher because it can be asymptomatic or cause minor symptoms
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spinal stenosis risk factors and presentation
``` Risk factors: Congenital narrowing of spinal canal Hyperparathyroidism Paget disease of bone Ankylosing spondylitis Cushing syndrome Acromegaly ``` Presentation: Pain in buttock or lower legs with or without back pain Often exacerbated by walking, lumbar extension Relieved by leaning forward, sitting or lying flat Gradual onset of uni/bilateral leg pain, numbness, weakness after walking predictable distance Less difficulty walking uphill rather than downhill Around half of patient have back pain usually bilateral and diffuse over the buttocks Neurogenic intermittent claudication: leg fatigue, motor weakness and leg numbness/paraesthesia Pain can be burning, cramping
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investigations for spinal stenosis, management and prognosis
``` Investigations: Clinical diagnosis - RULE OUT RED FLAGS Spinal exam Lumbar XR showing degenerative spine changes, narrowing disc space Lumbar MRI is GOLD STANDARD CT of lumbar spine ``` Management: NSAIDs Physiotherapy (forward flexion exercises) and epidural steroid injections Weight reduction PRN Neuropathic pain medications (amitriptyline, gabapentin or pregabalin) Surgery for those not responding to conservative measures (most improve) to decompress, laminectomy or implants Prognosis: Generally good for most patients, around half have no restriction of usual activities on long term follow ups
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ankylosing spondylitis
Inflammatory condition mainly affecting the spine causing progressive stiffness and pain Part of the seronegative spondyloarthropathy group of conditions relating to HLA B27 gene Other conditions include reactive arthritis and psoriatic arthritis Key joints affected in AS are the sacroiliac joints and joints of the vertebral column Inflammation causes pain and stiffness, can progress to fusion of the spine/sacroiliac joints Fusion leads to the classical bamboo spine Strong link with HLA B27 gene (90% patients have gene) and around 2% of people with this gene will develop AS. this is higher in those with family history of AS
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ankylosing spondylitis risk factors and presentation
Risk factors: Genetics (HLA B27 gene) Family history Usually presents in teens or 20s Presentation: Symptoms develop gradually over more than 3 months Lower back stiffness and pain Sacroiliac pain in buttock region Worse with rest and improved with movement Pain is worse at night and in the morning Often wakes them from sleep - fatigue Takes at least 30 minutes for stiffness to improve in the morning and gets progressively better with activity throughout the day Flare up symptoms of worsening pain and periods where symptoms improve Vertebral fractures may present as complication Associated presentation: Weight loss, fatigue Chest pain from costovertebral and costosternal joints Enthesitis (inflammation where tendons/ligaments insert) which may cause plantar fasciitis and achilles tendonitis Dactylitis Anaemia Anterior uveitis Aortitis Heart block from fibrosis of conductive system Restrictive lung disease from restricted chest wall movement Pulmonary fibrosis at upper lobes IBD
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investigations and management for ankylosing spondylitis
Spinal examination Schober’s test: part of spinal exam to assess mobility in spine. Patient stands straight, finds L5 vertebrae and mark points 10cm above and 5cm below this. Ask patient to bend forward as far as possible and measure the distance between the marked points. If this distance is LESS than 20cm this indicates restricted lumbar movement and helps diagnose AS Bloods: FBC, CRP, ESR raised HLA B27 gene test XR spine and sacrum: bamboo spine in later stages (vertebral body squaring, subchondral sclerosis and erosions, syndesmophytes ((bone growths where ligaments insert)) ossification, fusion of joints MRI may show bone marrow oedema in early disease before XR changes can be seen Management: NSAIDs for 2-4 weeks, if not improved with max dose then consider other NSAID Steroids during flares to control symptoms (oral or IM slow release or joint injections) anti-TNF meds like etanercept or monoclonal antibody against TNF like infliximab Secukinuab (anti-interleukin-17) recommended if response to all above is inadequate Physiotherapy - exercises and mobilization Avoid smoking Bisphosphonates for osteoporosis Complication management Surgery for deformities
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sciatica
Symptoms of pain, tingling and numbness arising from nerve root compression/irritation in the lumbosacral spine Symptoms typically extend below the knee from the buttocks, across back of the thigh to the outer calf, foot and toes Nerve root compression may be caused by: herniated IVD (90%), spondylolisthesis or spinal stenosis or cancers (more often metastases) Risk factors: Strenuous physical activity Whole body vibration (driving)
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sciatica presentation and complications
Presentation: Unilateral leg pain radiating below the knee to foot/toes Buttocks, back of thigh to outer calf Paraesthesia Muscle weakness in myotome Loss of tendon reflexes in single nerve root distribution Positive straight leg raising test: when lying supine, raising the leg while straight causes greater pain below the knee/more compression symptoms Extensor plantar response: lateral part of sole of foot is stimulated, toes extend and fan outwards which may indicate UMN lesion ``` Complications: Permanent nerve damage Psychosocial problems Loss of employment Prognosis is worse for women and those with greater functional impairment or pain ```
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sciatica investigations and management
Investigations: Clinical diagnosis Positive straight leg raising test: when lying supine, raising the leg while straight causes greater pain below the knee/more compression symptoms Extensor plantar response: lateral part of sole of foot is stimulated, toes extend and fan outwards which may indicate UMN lesion Red flags Management: Refer to neuro/orthopaedic surgery if there is progressive, persistent or severe neurological deficit Assess risk of back pain disability (STarT Back score of <3 = low risk of chronicity; 4+ and subscore of 3> medium risk of chronicity; 4+ and subscore of 4+ high risk chronicity) Quality of life, pain severity, function, psychological distress assessments Analgesia NOT gabapentinoids, antiepileptics, steroids or benzodiazepines or opioids for chronic sciatica (consider stopping these medications if already on them). NSAIDs have limited evidence. Educate on time course, self help measures, advice for staying active, resuming normal activities, returning to work ASAP High risk/those without improvement after 4-6 weeks of conservative measures refer for group exercise, CBT and physiotherapy Consider referral to sciatica specialist or low back pain services for epidural steroid/local anaesthetic injection if no improvement with other measurements Assess for radio frequency or spinal decompression may also be indicated for some people with sciatica when non-surgical management has not improved pain/function
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bone cysts and tumours
Benign lesions may cause pain, expansion into local structures, joint dysfunction and predispose to pathological fractures Secondary malignant tumours are much more common than primary malignant bone tumours
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benign bone tumours
osteoid osteoma: usually <1cm surrounded by dense osteoid. Often occurs in young adults. Most common sites are tibia, femur and vertebrae. Present with pain, worse at night and relieved by NSAIDs. XR shows radiolucency surrounded by dense bone. Local excision is curative
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benign cartilage tumours
Chondroma: Lesions can be single/multiple (Ollier’s disease) Appears in tubular bones of hands and feet XR shows well defined osteopenic area in medulla Lesion should be excised and bone grafted Osteochondroma: one of the most common benign bone tumours. Sessile or pedunculated lesions arising from the cortex of long bones adjacent to the epiphyseal plate. Can be single or multiple. Often presented in adolescence as cartilaginous overgrowth of epiphyseal plate, grows with the underlying bone. Presents as painless lump or occasionally joint pain. Problems include nerve compression (especially peroneal nerve), ankle diastasis and angular deformities. Malignant transformation to low-grade chondrosarcoma is more common with multiple osteochondromas and more proximal lesions Multiple hereditary exostosis is an autosomal dominant disorder with mild decrease in stature, and multiple osteochondromas. Commonly associated with leg discrepancy, knee and elbow angular deformities and other skeletal abnormalities
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benign fibrous tissue, bone marrow and vascular tumours
Fibroma: These occur in 40% of children aged >2 YO Usually asymptomatic Usually no treatment is needed except when it occupies >50% bone diameter when there is a need for curettage/bone grafting to avoid pathological fracture Bone marrow: Eosinophilic granuloma: Most common in boys aged 5-10 years occurs usually before age 30 Most often affects the skull with local pain, swelling, marked tenderness and warmth in the area Treatment with curettage/bone grafting, low dose radiotherapy or steroid injection Vascular: haemangioma
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giant cell tumour
Represents about 20% primary bone tumours Aggressive, locally recurrent tumours with low metastatic potential Found in a subarticular cancellous region of long bones. Most lesions are in close epiphyses around the knee or distal radius Only occurs AFTER closure of epiphyses Patients usually aged between 20-40 More common in women XR shows asymmetric rarefied area at end of long bone, cortex thinned or perforated Treated by local excision and grafting (often recurs) Gold standard treatment is wide excision and joint replacement to avoid recurrence Amputation if malignant or recurrent tumour
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malignant bone tumours
Osteosarcoma: most common primary bone malignancy in children. Highest incidence in 15-19 YO Slightly more common in boys Occurs in metaphysis of long bones. Most common site is around the knee or proximal humerus Often presents as a relatively painless tumour. Destroys the bone and spreads into surrounding tissue, rapidly metastasises to the lung XR shows a combination of bone destruction and formation. Soft tissue calcification produced sunburst appearance Disease free survival rate is 55-75% with surgery and effective chemotherapy Pulmonary metastases particularly problematic and associated with poorer prognosis
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malignant cartilage, fibrous tissue and bone marrow, vascular tumours
Chondrosarcoma: One of the most common bone sarcomas of adulthood Most common between 30-60 YO May arise from pre-existing lesions or can be primary Usually associated with dull, deep pain Radiographs may show invasiveness and soft tissue extension Occurs in two forms: central (tumour in pelvis/proximal long bones) and peripheral (in cartilaginous cap of osteochondroma) Tend to metastasise late Wide local excision often possible Fibrous tissue: fibrosarcoma Bone marrow: myeloma Ewing’s sarcoma: Primitive neuroectodermal tumour (PNET) thought to arise from mesenchymal stem cells. Is rare, affecting 30 children per year in the UK Most common in white caucasians under age 25 (median age 15) Slightly more common in men Presents with swelling or mass, pain, erythema, malaise, anorexia, weight loss, fever, paralysis, incontinence Ix: XR, biopsy, FBC, LFTs, CT/MRI, bone scintigraphy Mx: needs long term support from MDT; chemotherapy first line, radiotherapy in conjunct, peripheral blood stem cell harvesting, surgery oten needed to remove tumour Overall 5 year survival rate is 50% Vascular: angiosarcoma Uncertain: malignant giant cell tumour
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metastatic secondary tumours of bone
Most common bone malignancies especially in the elderly Usually multiple but can be solitary Most common primaries are breast, prostate, lung, kidney and thyroid Wilms tumour and neuroblastoma are the most common metastatic lesions in childhood Most present with pain, swelling, localised tenderness, rapid growth and erythema May cause pathological fractures Ix: XR, MRI/CT, bone scan, biopsy, Ix for primary lesions
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MSK carcinoma investigations and grading
Investigation for ALL: XR MRI Bone biopsy to confirm Grading: Low grade: cells are well differentiated and slow growing High grade: cells are poorly differentiated, grow quickly and more likely to spread Stage IA - the cancer consists of low-grade cells and is totally within the bone. There is no spread to other parts of the body. Stage IB - the cancer consists of low-grade cells but has grown through the wall of the bone. There is no spread to other parts of the body. Stage IIA - the cancer consists of high-grade cells and is totally within the bone. There is no spread to other parts of the body. Stage IIB - the cancer consists of high-grade cells but has grown through the wall of the bone. There is no spread to other parts of the body. Stage III - the cancer is any grade but has spread to other parts of the body
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MSK cancers management
2WW to bone sarcoma reference centre Biopsy Immobilise or splint any pathological fractures to prevent tumour dissemination of tumour cells into surrounding tissues Follow up: monitor for local recurrence of metastatic disease (physical exams, CXR, CT scns etc.) After chemotherapy completion assess every 6 weeks-3 months for the first 2 years, every 2-4 months for years 3-4 and every 6 months for years 5-10 and thereafter
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sarcoma vs carcinoma
Sarcomas: MSK originally from the mesoderm Repair is slow (especially in bone, ligaments, tendons) Recovery is based on weeks rather than days Sarcomas are different from carcinomas as patients are younger, more vascular (sarco- fleshy excrescence) and grows more rapidly Metastases are mainly haematogenous .e.g. metastases to the lung Grade is part of staging i.e. TNMG instead of TNM in carcinoma Forms in myoepithelial cells which make up connective tissues like bones, muscles, fat, blood vessels and lymphatic vessels Muscles and NS are the most differentiated tissues in the body; cancer is not common; when they are lost replacing them is a large challenge for the body Pancreatic, prostate, breast cancers are most likely to metastasise to bone Carcinoma Forms in epithelial cells which make up lining of tissue organs
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osteomalacia vs osteoporosis
osteomalacia: imbalance between supply and demand of vitamin D bone mineralisation decreases causing soft bone easy to bow bone pains and muscle weakness increased ALP with decreased Ca and phosphate XR shows looser's zone/pseudofractures treated with vitamin D replacement ostoporosis: imbalance between osteoblast and osteoclast activity, decreases bone mass, impaired microarchitecture of bone bone looks hard but is brittle and easy to fracture often asymptomatic but may show kyphosis or pathological fractures Ix with DEXA and BMD calculation (T score
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osteomalacia vs rickets
osteomalacia is the result of vitamin D defieciency AFTER fusion of epiphysis in adults. less severe presentation rickets is the result of vitamin D deficiency occurring BEFORE fusion of epiphyses (during bone growth) in children and is a lot more severe in presentation