MSK Flashcards
polymyalgia reumatica and risk factors
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
polymyalgia reumatica presentation
> 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
polymyalgia reumatica investigations
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!!
polymyalgia reumatica management, prognosis and complications
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
fibromyalgia
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)
fibromyalgia risk factors and presentation
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
fibromyalgia investigations and management
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
gout
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
phases of gout pathology and risk factors
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
presentation of gout
Acute pain in joint
Swelling
Erythema
Typically in MTP joints but can occur in knees, midtarsal joints, wrists, ankles, hands and elbows
Gout investigations
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
Gout management
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
Gout complications
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
osteoarthritis
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
osteoarthritis risk factors
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
osteoarthritis presentation
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
osteoarthritis investigations
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
osteoarthritis management
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
osteoporosis
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
postmenopausal osteoporosis
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.
risk factors for osteoporosis
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
osteoporosis presentation
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
osteoporosis investigations
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
osteoporosis management and complications
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
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
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
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
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
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
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)
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
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
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.
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
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
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
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)
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
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
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
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
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)
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’
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
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
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
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
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
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
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
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
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
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
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
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
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)
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
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)
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
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
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)
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
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
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
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.
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.
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.
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
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
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
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
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
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
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
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)
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
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
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!!
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
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
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
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
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
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
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
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
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
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)
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
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
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)
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
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
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!
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
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)
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
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
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
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
