MDD Flashcards
What are the contraindications for joint surgery?
It is generally contraindicated to perform surgery on an actively infected or recurrently infected joint
Complications of joint / soft-tissue surgery
Wound infection (1% elective; 20% open fractures)
DVT (~50% total hip/knee replacements)
MI
Local neuromuscular injury
Compartment syndrome
Periprosthetic fracture
Complex regional pain syndrome
Carpal Bones
“Some Lovers Try Positions That They Can’t Handle”
Proximal Row (lateral to medial):
- Scaphoid
- Lunate
- Triquetrum
- Pisiform
Distal Row (lateral to medial):
- Trapezium
- Trapezoid
- Capitate
- Hamate
What forms the carpal tunnel?
What are the contents?
the flexor retinaculum attaches to both sides of the carpal bones, forming the carpal tunnel.
The carpal tunnel contains:
- FPL, FDP, FDS tendons
- MEDIAN NERVE !
Phalanges
= are the bones of the fingers.
The thumb has a proximal and distal phalanx
The rest of the digits have proximal, middle and distal phalanges.
Radiocarpal joint
= a synovial joint, formed by:
- Distally – The proximal row of the carpal bones (except the pisiform).
- Proximally – The distal end of the radius, and the articular disk.
Why is the ulna not a part of the wrist joint?
The ulna articulates with the radius, just proximal to the wrist joint, at the distal radioulnar joint.
What are the ligaments the wrist joint?
What are their functions?
Palmar Radiocarpal
Dorsal Radiocarpal
Ulnar Collateral
Radial Collateral
These stabilise the wrist, and prevent excessing deviation.
The palmar radoiocarpal assists in supination
The dorsal radoiocarpal ligament assists in pronation.
Vascular supply to the wrist
The wrist joint receives blood from branches of the dorsal and palmar carpal arches, which are derived from the ulnar and radial arteries
What are the possible movements of the wrist?
- Flexion
- Extension
- Adduction
- Abduction
how does the wrist flex?
Produced mainly by the flexor carpi ulnaris, flexor carpi radialis
Assistance from the flexor digitorum superficialis.
How does the wrist extend?
Produced mainly by the extensor carpi radialis longus and brevis, and extensor carpi ulnaris,
Assistance from the extensor digitorum.
How does the wrist adduct?
Produced by the extensor carpi radialis and flexor carpi ulnaris
How does the wrist abduct?
Produced by the APL, flexor carpi radialis, extensor carpi radialis longus and brevis.
Extrinsic muscles of the hand
= located in the anterior and posterior compartments of the forearm.
They control crude movements and produce a forceful grip
Intrinsic muscles of the hand
= located within the hand itself.
They are responsible for the fine motor functions of the hand.
These include the adductor pollicis, palmaris brevis, interossei, lumbricals, thenar and hypothenar muscles
What make up the thenar muscles?
What movements are they responsible for?
What is their innervation?
They are responsible for the fine movements of the thumb
All innervated by median nerve
Opponens Pollicis => opposition of thumb
Abductor Pollicis Brevis => abducts thumb
Flexor Pollicis Brevis => flexes MCP joint of thumb
What make up the Hypothenar Muscles?
What movements are they responsible for?
What is their innervation?
All innervated by ulnar nerve
Flexor Digiti Minimi Brevis => Flexes the MCP joint of the little finger.
Opponens Digiti Minimi => opposition of little finger
Abductor Digiti Minimi => abducts little finger
Lumbricals - movement and innervation
there are 4 lumbricals in the hand, each associated with a finger
=> Flexion at the MCP joint and extension at the interphalangeal (IP) joints of each digit
The lateral two lumbricals (of the index and middle fingers) are innervated by the median nerve. The medial two lumbricals (of the little and ring fingers) are innervated by the ulnar nerve.
Interossei muscles - movements and innervation
Located between the metacarpals.
They can be divided into two groups:
- Dorsal interossei:
=> Abduction
=> Also assist the lumbricals in flexion at the MCP joints and extension at the IP joints. - Palmar interossei.
=> Adduction
=> Also assist the lumbricals in flexion at the MCP joints and extension at the IP joints.
Both groups innervated by ulnar nerve.
What are the muscles of the palm?
- Palmaris Brevis
- Adductor Pollicis
A-delta nerve fibres
Give rise to perception of sharp, immediate pain.
Myelinated fibres; fast conduction velocity
C nerve fibres
Give rise to slower onset, prolonged pain.
Unmyelinated fibres; slower conduction velocity
these are the predominant pain sensory afferent fibres.
WHO Pain ladder steps
- Non-opioid +/- adjuvant
- Weak opioid +/- non-opioid +/- adjuvant
- Strong opioid +/- non-opioid +/- adjuvant
Indications for paracetamol
mild-moderate pain and pyrexia.
Paracetamol dosing
Dose is 1g PO/IV q.d.s to a maximum of 4g/day.
This dose is reduced in patients <50kg.
3g/day maximum is recommended if there is a risk of hepatotoxicity
NSAIDs - mechanism of action
= inhibition of COX enzymes, which normally promote the production of prostaglandins and thromboxane.
Anti-inflammatory and analgesic effects (good for inflammatory pain), with some antipyretic effect.
COX-1 vs COX-2 enzymes
COX-1 is expressed in most tissues, with the PGs produced involved in tissue homeostasis
=> Platelet aggregation, renal blood flow autoregulation, GI protection
COX-2 is induced in active inflammatory cells by IL-1 and TNF-alpha
=> Sensitises nociceptors to inflammatory mediators peripherally
=> Sensitises afferent pain fibres in dorsal horn centrally.
side effects of NSAIDs
• Dyspepsia & gastric ulceration
• Bronchospasm (in “aspirin sensitive asthmas”)
• Renal insufficiency
• Cardiotoxicity
• Decreased platelet count
• Skin reactions
Absolute contraindications for NSAIDs
- Severe heart failure
- History of GI bleeds/ulceration
Cautions for NSAIDs
asthma,
the elderly,
coagulopathies
renal/hepatic/cardiac impairment
COX-2 Selective inhibitors
Less GI side effects
Licensed for use in RA/OA, however risk of serious adverse cardiac events needs to be considered
Opiates - mechanism of action
act on mu-opioid receptors in the CNS and throughout the body, decreasing neuro-excitability.
Side effects of opioid analgesics
- Respiratory depression
- Nausea & vomiting
- Constipation
- Sedation/depression of cough reflex
- Gall bladder contraction (not recommended in gallstone disease)
Tramadol also has MAOI effects, and thus can lead to serotonin syndrome if used in conjunction with other serotonergic drugs.
Absolute contraindications for use of opioids
- Acute respiratory depression
- Acute alcoholism
- Risk of paralytic ileus
- Raised ICP
What is important to consider prescribing alongside opioids?
Anti-emetics
=> Metoclopramide is usually co-prescribed
Laxatives
=> Senna & lactulose are also co-prescribed
Why should anti-emetics and laxatives also be prescribed with weak opioids?
Weak opioids (codeine/tramadol) have full-strength opioid side effects so laxatives and anti-emetics should be prescribed.
Managing opioid overdose
In patients over 12 with respiratory depression due to opioid administration, give 400 micrograms naloxone IV.
If no response after 1 minute, give a further 800 mcg.
If no response after 2 minutes, give a further 800 mcg.
2mg / 4mg doses can be given in severely poisoned patients
What are the main indications for use of a PCA?
= post-op or oncology.
Non-drug analgesia in MSK medicine?
Splinting
=> Very effective analgesic technique in trauma.
Cold therapy:
=> Very effective around joints post-surgery.
TENS
=> Electrical current applied via hand-held generator to activate nerve fibres in tissues below.
Acupuncture:
=> Can be effective in certain conditions.
CBT
What are disease modifying anti-rheumatic drugs (DMARDs)?
Include methotrexate, sulfasalazine, hydroxychloroquine, penicillamine and gold compounds.
Can reduce the pain score, disability score and RF level
Their clinical effect is often slow, thus steroids are used to cover the induction phase.
Combination therapies are generally superior to monotherapy.
DMARD - methotrexate
= Folic acid antagonist
Quickest onset of action of DMARDs
Once weekly dosing (oral/IM)
=> Folic acid should be taken on the other 6 days of the week
Not suitable in pregnancy, or in males trying to conceive (stop for 6 months before)
What is the 1st line DMARD ?
= Methotrexate
What is important to remember when prescribing methotrexate?
Once WEEKLY dosing (oral/IM)
Folic acid should be taken on either the other 6 days of the week or one other day
Patients should be educated on signs of toxicity:
=> Bruising, infection, shortness of breath
Common SEs of methotrexate
nausea, headaches, tingling
Monitoring for patients on methotrexate
FBC, LFT, U&Es are required every 10 weeks once settled on the drug.
DMARD - Sulfasalazine
Response time, monitoring, SEs
Takes ~8 weeks to have a clinical response.
FBC, U&E, LFT should be monitored monthly for the 1st 3 months.
SEs – nausea, dyspepsia, rashes, blood dyscrasias, azoospermia, yellow-orange discolouration of urine/contact lenses.
DMARD - Hydroxychloroquine
Response time, monitoring, SEs
Least effective but least toxic
Takes 6 weeks for a clinical response
Only monitoring required = baseline visual acuity and annual re-check
SEs – rash, GI disturbances, peripheral neuropathy, retinal damage.
DMARD - use of biologics and their SEs
Anti-TNF agents are the most common (e.g. infliximab, etanercept)
Adverse effects = opportunistic infections, non-melanoma skin cancers and injection site reactions
Infusion reactions can also occur, so many are given in hospital (at least initially)
Contraindications/cautions for use of biologics
= active infection, latent TB, malignancy, pulmonary fibrosis, severe heart failure.
=> CXR required prior to commencing treatment
Corticosteroids - Mechanism of Action
Act by inhibiting transcription of COX-2, cytokines and ILs
Also increase annexin-1 production, which has anti-inflammatory effects.
Systemic Corticosteroids - SEs
There are widespread side effects associated with steroids:
- Infection / poor wound healing
- Peptic ulceration
- Acute adrenal insufficiency upon withdrawal (thus dose tapered down)
- Cushing’s Syndrome
- DM
- Osteoporosis
- Avascular necrosis
- Psychological effects (depression, psychosis)
- Inter-scapular fat pad (“buffalo hump”)
What is important to co-prescribe with long-term steroids?
Any patient on long-term corticosteroids should be co-prescribed gastroprotection (most commonly PPIs), vitamin D and bisphosphonates.
What is the preferred route of steroids in rheumatology?
Can be given orally (prednisolone), but many rheumatology centres prefer IM (methylprednisolone).
=> IM has a depot effect that self-tapers down.
Intra-articular steroid injections
Can have a diagnostic and therapeutic effect
=> the preparation often contains local anaesthetic, so if the pain resolves within a short period of time then we can be reasonably confident that the pain is coming from the structure injected.
Do not repeat more than 3x in 6 months
There can be systemic absorption and side effects
Injections may be into joints or peri-articular structures to provide pain relief.
What can be used for non-pharmacological pain management in MSK medicine?
Education
Physiotherapy
Physical Treatments - heat/cold, aids, splints
Coping strategies - e.g. relaxation techniques
What are the most common primary cancers that metastasise to the bone?
“BLT KP nuts”
Breast, Lung, Thyroid, Kidney, Prostate
What are the different patterns that bone metastases can take?
Can involve a mixture of bone resorption and bone formation and can thus take on one of three patterns, depending on the dominant process:
- Lytic (osteolytic) metastases
- Sclerotic (osteoblastic) metastases
- Mixed lytic and sclerotic metastases
Where are the most common locations for bony metastases?
• Vertebrae
=> Lumbar spine more than thoracic spine and cervical spine
• Pelvis
• Proximal femur
• Proximal humerus
• Skull
(Metastases distal to the elbow and knee are distinctly uncommon)
Bone mets - symptoms
• Unremitting, dull pain – may be sharp on weight bearing; worse at night
• Pathological fractures
• B symptoms
More rarely – spinal cord compression (leading to radicular pain and autonomic dysfunction).
Bone mets - O/E
• Bone tenderness
• Reduced ROM of the joints
• Local lymphadenopathy
Bone mets - investigations
Skeletal radioisotope scans – shows mets as “hot areas” before radiological changes occur
Skeletal XR
=> Sclerotic or lytic areas once the tumour reaches a certain size.
CT/MRI
=> To define bone loss, marrow involvement and tumour extension
=> Imaging for location of the primary tumour.
General bloods +/- tumour markers
Management of bone pain from bone metastases
Establish the primary diagnosis + treat
Analgesia / local radiotherapy to control the pain
Bisphosphonates to reduce fracture risk
Prophylactic surgical stabilisation may be indicated to prevent pathological fractures.
What is multiple myeloma ?
= a type of bone marrow cancer.
It’s called multiple myeloma as the cancer often affects several areas of the body, such as the spine, skull, pelvis and ribs.
Multiple myeloma - presentation
Bone destruction leads to pathological fractures
=> Particularly in the vertebrae, leading to backache.
Signs of bone marrow infiltration and renal impairment
=> Can present with CKD signs, recurrent infections, signs of anaemia, hypercalcaemia, etc.
Multiple myeloma - X-Ray findings
XR will show “punched-out” lytic lesions.
Multiple myeloma - Mx of bone pain
Radiotherapy for local disease control
Spinal decompression and fusion if necessary
Osteosarcoma
= Malignant tumour of osteoblasts
Grow rapidly to invade surrounding soft tissues, metastasising early
Often advanced at presentation
Mets are often to the lungs.
Osteosarcoma - prognosis
Very poor prognosis (5-10% 5-year survival)
Osteosarcoma - who gets it?
Occurs in children, most commonly around the knee.
Rarely can occur in the elderly, associated with long-standing Paget’s
Chondrosarcoma
Malignant cartilage-forming lesion.
Grows slowly and metastasises late
Can be large at presentation, but generally stay within a defined border.
Occur in adults, most commonly around the pelvis.
Chondrosarcoma - presentation
Pain / mechanical symptoms / occasionally a pathological fracture.
Benign primary tumours of bone
osteoma, chondroma, and osteochondroma
Bone tumours - Ix
Further imaging and biopsy are always indicated to determine the nature of a lesion detected on XR (2WW pathway)
Bone tumours - Mx
Generally life > limb:
En-bloc resection with adjunctive chemo/radiotherapy is commonly seen.
What is a person’s functional capacity?
= a person’s fullest potential
What is a person’s functional performance?
= the level a person is currently at
What is Participation Restriction?
When the person is limited in participating in society as they want to (participation is lost/reduced)
What is rehabilitation?
= the development of a person to their fullest potential, within the limitations of their underlying condition and the resources available.
It is goal-directed - need to identify the person’s specific requirements and activity limitations.
REPAIR model for rehabilitation
- Review of pathology and impairment
- Environment
- Participation
- Activity
- Important others
- Risk
Paget’s disease of Bone - pathophysiology
Involves excessive uncontrolled resorption of bone by large abnormal multinucleated osteoclasts.
The destruction of cortical and trabecular bone comes in waves, with each wave followed by an osteoblastic response, occurring in a haphazard fashion.
=> Bone architecture becomes distorted
Although there may be an increase in bone bulk, it is paradoxically weaker than normal.
The new bone has a characteristic woven, non-lamellar pattern, with fibrosis of the marrow spaces
Paget’s Disease of the Bone - Presentation
Up to 80% are asymptomatic
=> Diagnosis may follow an incidental finding on XR or LFTs (raised ALP).
Symptoms:
- Waxing and waning bone pain
- Bone deformities (bowed tibia / skull changes)
- Cranial nerve palsies due to compression (classically CNVIII)
- Cardiac failure due to increased bone blood flow.
What is the “textbook” presentation of Paget’s Disease of bone?
- Bone pain,
- Pathological fractures
- Deafness (CNVIII palsy)
Paget’s Disease of bone - Ix
Bloods
=> ALP raised, calcium and phosphate normal.
(Can be a mild hypercalcaemia in widespread disease)
Urine
=> Raised hydroxyproline due to increased bone turnover
XR
=> Variable presentation, with lytic and sclerotic lesions
Bone scans
=> Used to show extent of bone involvement – but cannot differentiate between Paget’s and sclerotic metastases.
Paget’s Disease of Bone - Mx
Simple analgesics
Bisphosphonates for disease modification
Monitor serum ALP as a disease marker
Asymptomatic patients may be treated if there are significant risk factors for complications
Surgery may be required to deal with secondary joint disease or neurological complications.
Indications for elective joint replacement surgery
pain / stiffness leading to a loss of function.
Absolute contraindications for joint replacement surgery
untreated joint sepsis
Relative contraindications for joint replacement surgery
Young age,
Co-morbid diseases (including obesity).
Total Hip Replacement - indications
Elective replacement in OA
Emergency replacement (young/fit patient) – Garden 3/4 intracapsular NOF #
What is a total hip replacement?
Has 2 components:
=> Acetabular component
=> Femoral component
Hip Hemiarthroplasty - indications
Emergency replacement of Garden 3/4 intracapsular NOF # (unless particularly young/fit)
What is a hemiarthroplasty of the hip?
Has only the femoral component
=> Bipolar – an endo-prosthetic “bipolar” head component and an inner metal bearing
=> Unipolar – a large single endo-prosthetic head component
Can be cemented/uncemented
What are the benefits of cementing a hip replacement?
The femoral component will be more uniformly and more securely fixed within the femoral canal
What are the risks with cementing a hip replacement?
Cement confers the risks of cardiac arrhythmias and cardio-respiratory compromise, secondary to fat embolism and cement reaction phenomena.
Complications of hip replacement
- Leg length discrepancy
- Dislocation (highest risk in the first 3 months)
- Infection
- Periprosthetic fracture
- Persistent pain
- Polyethelene wear of the acetabular compartment (if THR)
- Neurovascular injury
Infection of hip replacement
A rare but devastating complication
=> Joint-salvage rates are 30% if caught early.
Often presents subclinically, with little systemic upset.
If suspected, the joint will be aspirated in aseptic conditions (ideally on 3 separate occasions).
Mx – usually involves removal of the prosthesis and lengthy courses of ABX to clear the infection before a new prosthesis can be inserted.
What is the definition of osteoporosis?
= a disease characterised by reduced bone mineral density and microarchitectural deterioration of bone tissue, leading to increased bone fragility and an increased risk of fracture
WHO Definition = bone mineral density >2.5 SDs below that of a young adult male (T-score)
Osteopaenia vs osteoporosis
T- score below -2.5 = osteoporosis
T score between -1 and -2.5 = osteopaenia
Osteoporosis - pathogenesis
In normal individuals, bone mass increases during childhood to reach a peak between 20-30, when there is a period of consolidation before it falls thereafter.
Women have an accelerated phase of bone loss after menopause, as a result of oestrogen deficiency.
Osteoporosis - RFs
Age
Female Sex
Genetics
=> 80% of peak bone mass determined by genetics, also rate of bone turnover.
Low peak bone mass:
=> Limited early exercise
=> Limited early calcium intake
=> Low BMI in childhood
Disuse – leading to “disuse atrophy”
=> E.g. following a fracture
Steroid use
Endocrine - Cushing’s, hyperPTH, hyperthyroid, hypogonadism
Chronic inflammatory disease / neoplastic disease
Smoking and alcohol
How do corticosteroids cause osteoporosis?
The risk is directly related to dose/duration of therapy.
Steroids cause decreased intestinal calcium absorption and increased renal calcium excretion, leading to secondary hyperparathyroidism.
This is combined with direct inhibition of osteoblast activity and stimulation of osteoblast apoptosis.
Osteoporosis - presentation
Clinically the disease is mainly asymptomatic and often picked up incidentally if patients have an X-ray for another condition.
If symptoms occur, they may be:
- Fragility fractures
- Back pain
- Height loss
- Kyphosis
How does osteoporosis appear on X-ray?
The bones will appear more radiolucent than normal and loss of bony trabeculae.
Where are the most common sites for fragility fractures?
wrist, NOF, spine (crush/wedge #)
What is the gold-standard investigation for osteoporosis?
measuring bone mineral density (BMD) with DEXA scan
Where is a DEXA scan measured?
at the lumbar spine and iliac crest.
T-score vs Z-score
T-score = how many standard deviations the BMD deviates from a young adult male
Z- score = how many SDs BMD deviates from an age-matched control
Osteoporosis - Ix
DEXA scan to confirm
Once osteoporosis has been confirmed:
- History – to identify predisposing causes.
- Physical examination – including a search for endocrine disease and inflammatory disease
- Bloods – calcium, phosphate, TFTs, ESR
- Sex hormone panel in men and amenorrhoeic women below 50.
Further studies requested based on clinical suspicion
Screening for osteoporosis / fragility fracture
The FRAX tool should be used in GP for patients over 50 to estimate the risk of fragility fracture
Uses multiple demographic details to give “high”, “intermediate” or “low” risk of fragility fracture.
Management based on FRAX score
If the 10-year risk is low – reassurance
If 10-year risk is high – treatment is advised.
If 10-year risk is intermediate – DEXA scan should be offered.
How should patients with osteopenia be managed?
Patients with osteopaenia should be given advice on lifestyle factors:
- Stop smoking and limit alcohol
- Increase exercise and dietary calcium intake
Repeat DEXA scans should be offered to this group.
Management of osteoporosis
Patients with BMD in the osteoporotic range should be offered treatment:
- Weekly bisphosphonates (alendronic acid) are 1st line.
- Vitamin D should also be given as an adjunct for those not exposed to much, as well as calcium if the person’s calcium intake is judged to be inadequate.
=> Adcal is a combined calcium and VitD supplement. - HRT should be considered in women with premature menopause to reduce the risk of fragility fractures (and for the relief of menopausal symptoms).
- Testosterone replacement can be given in males with hypogonadism.
Fracture risk and BMD should be re-measured at 2 years.
How do bisphosphonates work?
What are some side effects?
Act to decrease bone resorption and allow mineralisation of existing bone to increase.
Can give troublesome GI side effects
A rarer complication is osteonecrosis of the jaw.
What are some more specialist treatments for osteoporosis?
Calcitonin – osteoclast inhibitor
Recombinant PTH (daily s.c. injection, beneficial due to the daily peaks and troughs mimicking a circulating hormone, rather than sustained elevation as in hyperPTH)
What is osteomalacia?
What causes it?
inadequate bone mineralisation (i.e. soft bones), usually caused by vitamin D deficiency in adults.
=> Rarer causes include hypophosphataemia, bisphosphonates, fluoride or aluminium intoxication.
Osteomalacia - presentation
Characterised by bone pain, bone fragility and fractures.
Often more insidious in onset, presenting with malaise and general weakness.
Rickets is the syndrome resulting from osteomalacia in the growing skeleton.
=> These patients develop bone deformity in addition to the above features.
How does osteomalacia tend to present in the UK?
Full-blown osteomalacia is rare in developed countries, but subclinical disease is still common in patients with poor diet, or little sun exposure.
=> Features in adults will present insidiously, with many cases only picked up on biochemistry.
Basics of Vit D metabolism in the body
Vit D (cholecalciferol) can be ingested directly (high levels in oily fish, eggs, and fortified cereals)
Most is synthesised from 7-dehydrocholesterol in the skin, providing there is adequate UV sunlight exposure.
Ingested/synthesised Vitamin D is hydroxylated in the liver to form 25-hydroxycholecalciferol. There is a second hydroxylation in the kidney, to produce 1,25-hydroxycholecalciferol (“Calcitriol”)
Calcitriol circulates as a hormone in the blood to help maintain skeletal calcium balance
What is the main action of calcitriol?
Main action = promotion of calcium absorption from the intestines
Causes of Vitamin D deficiency
Inadequate dietary intake (rare in developed world, but can occur in vegans/patients with malabsorptive disease)
Inadequate UV exposure for synthesis of VitD – e.g. housebound patients, muslim women.
Renal disease – e.g. CKD
Liver disease – a rare cause
Drugs
Osteomalacia - Ix
Bloods:
- U&Es – screen for renal anomalies
- ALP – raised (indicates increased osteoblast activity)
- Plasma calcium – normal/low
- Serum phosphate – low
- Serum PTH levels – high
- Serum 25-OH-D – low
X-Ray:
- Often normal, may show “looser zones” of defective mineralisation in long bone/pelvis/ribs.
- In children, the pathognomic feature is widening of the epiphyseal plate.
An ILIAC CREST BIOPSY may be necessary if tests do not confirm diagnosis.
Osteomalacia - Mx
Oral VitD replacements – high dose for 4 weeks, then maintenance.
=> IV if the issue is malabsorption
=> Activated form if the issue is renal/hepatic disease
The disease usually responds fairly rapidly to a restoration of VitD
Timings of cell death in osteonecrosis
Bone marrow cells die within 12 hours
Bone cells (osteoblast, osteoclast, osteocytes) die between 12-24 hours
Osteonecrosis in shaft of long bone
typically described as bone infarction
only involves the trabecular bone and bone marrow in the medulla (the cortex has blood supply from the periosteum).
Osteonecrosis in the epiphysis
called avascular necrosis
this may involve the cortical bone as the epiphyses are covered by cartilage and thus do not have periosteal supply.
Which bones are more susceptible to osteonecrosis?
• The head of femur – following fracture NOF of hip dislocation
• The proximal scaphoid – following displaced wrist fracture
• The lunate – following dislocation
• The body of the talus – after talus neck fracture
Causes of osteonecrosis
Interrupted arterial supply (e.g. fractures)
Interrupted venous drainage and retrograde arterial stoppage (e.g. thrombosis, or bone marrow swelling compressing vessels).
Osteonecrosis - RFs
Fracture – e.g. intracapsular NOF fracture, scaphoid fracture
Idiopathic – e.g. Perthe’s disease, AVN of femoral head
Bone marrow infiltration (malignancy)
Alcohol abuse
Cushing’s / exogenous corticosteroids / chemotherapy
Infection – septic arthritis
Osteonecrosis - presentation
Osteonecrosis is often well advanced at presentation.
Symptoms are:
• Pain
• Stiffness
• Swelling in a local joint or over the bone (depending on location)
Osteonecrosis - Investigations
X-ray will show a distinctive segment of increased bone density (due to new bone formation), however this will only be present after 6 months.
MRI/radionucleotide scans can show earlier changes.
Osteonecrosis - Mx
- Eliminate the cause
- Prevent complications (e.g. fracture)
- Potentially surgical intervention
What are the indications for lower limb amputation?
Vascular disease (= most common cause).
Infection
Trauma
Neoplastic disease
What are the two major lower limb amputation levels?
Which are more common?
- Transtibial (below knee)
- Transfemoral (above-knee)
Transtibial amputations are the most common
=> ratio of 2:1 – TTA:TFA
What is the goal when deciding a level to amputate?
= to amputate at the most distal level that will remove the diseased tissue, whilst preserving functional residual limb length and creating the best environment for rapid return of mobility and function.
The ideal residual limb post-amputation should be…
• Appropriate length
• Knee joint preserved (if sound)
• Smooth, bevelled bone
=> To prevent bony pressure points
• No soft tissue excess / constant volume
• Healthy sensate skin
• Healed wound with mobile scar
• Good muscle power
• Full movement at proximal joints
• Free of pain?
Trans-tibial Amputation
Have markedly reduced peri-operative mortality and better prognosis.
~70% of TT amputees will walk again
=> Walking with a TT prosthesis is much less energy consumed than TFA.
Trans-femoral Amputation
most commonly occur in severe vascular disease.
Only ~40% of adult Transfemoral amputees will walk again
Why do trans-femoral amputations not do as well when it comes to walking again?
Because multiple joints (Knee and ankle) are being replaced with a prosthesis, the patient has to cope with more challenges to balance due to near total loss of proprioceptive and sensory input from the affected leg.
Amputation - Stump Pain
= Pain in the residual portion of the limb
Pathophysiology is unclear
Generally resolves with wound healing, but 15-30% report persistent pain
Other causes - prosthesis causing damage, stump pathology, referred pain from back/sciatica/arthritis in nearby joint.
Phantom Limb Sensation
= any sensation felt in the amputated limb, except pain.
Phantom Limb Pain
= Painful sensation of the missing limb
Occurs in 55-85%
Develops a few days after the amputation, and usually improves with time but may be permanent
Phantom Limb Pain - Mx
1st line Tx = PREVENTION
=> Pre and peri-op epidural to get the pain under control.
For a patient with established phantom limb pain:
- Antidepressants/anticonvulsants,
- Massage of contralateral limb
- Psychological support
Who can get a prosthesis?
After an amputation, everybody is entitled to an assessment for a prosthetic limb should they want one.
The assessment is performed by the specialist MDT.
A prosthetic limb will then require intensive physiotherapy and gait training for the patient to become mobile on that limb.
What does suitability for a prosthesis depend on?
Cognitive ability
Motivation
Previous mobility level
Expectations / goals
Physical strength
Condition of contralateral leg
Wound healing post-surgery
Co-morbidities
Hopping with a prosthesis
Hopping is not generally promoted, due to the potential for falls, damaging the remaining foot, and increased joint pressure on the “hopping side”
Associated complications with prosthetic limbs
Pressure sores
Skin rashes/allergies
Neuroma development
Contralateral joint issues
Poor patient acceptance (doesn’t meet expectations).
Psychological Support for amputees
Around 75% of people with amputation experience low mood +/- anxiety.
Psychological function can deteriorate over time and many find psychological support more useful later in their rehabilitation journey.
Mild Traumatic Brain Injury
GCS 13-14
Post-traumatic Amnesia <6 hrs
LOC <15 minutes
Moderate Traumatic Brain Injury
GCS 8-12
Post-traumatic Amnesia 6 – 24 hours
LOC 15 mins to 6 hours
Severe Traumatic Brain Injury
GCS <7
Post-traumatic Amnesia - 24 hours to one week
LOC 6 – 48 hours
Acute Brian Injury Syndromes
Coma (2-4 weeks)
Brain death
Vegetative state
Minimally conscious state
Concussion
Post-concussion syndrome
“Locked in syndrome”
When is a vegetative state considered permanent?
Considered permanent if lasts >1 year in a TBI
(>6 months in anoxic brain injury)
Post-traumatic Amnesia
Used to categorise severity of TBI
Main feature = inability to remember events; also confusion and disorientation.
Most recover over hours to days.
Often have no recollection of the accident
What is a good structure for a post-op assessment of a joint replacement patient?
IMPOTENCE
Introduction
Mental State
Pain
Observations
Thromboprophylaxis
Eating & Drinking & Elimination
Neurovascular Status
Cut
Exercise
Post-op Assessment - Introduction
Name, age
What surgery?
How many days post-op (operation day = day 0)
Anaesthetic type? +/- sedation
Intra-operative complications?
Post-op Assessment - Mental state
Alert & orientated?
If not, why?
=> GCS / AVPU
=> consider AMT
Post-op Assessment - Pain
Where is the pain? – SOCRATES (consider other sites!!)
Is analgesia effective?
Consider ice packs (good for knees)
N&V – anti-emetics?
Laxatives
Post-op Assessment - Obervations
NEWS = 0? If not, why?
+/- CVS / resp exam
+/- Glucose measurement
Post-op Assessment - Thromboprophylaxis
Calves SNT?
Compression stockings
LMWH/aspirin?
Foot pumps?
Mobilise ASAP
Post-op Assessment - E&D & Elimination
Diet & Fluids
Fluid balance chart?
Passing urine / catheter (colour & amount)
?Bowels opened – if not, passing flatus?
Bowel sounds / abdo SNT
Post-op Assessment - Neurovascular Status
Check distal neurological & vascular status and document
Consider anaesthetic & surgery (e.g. nerve block still ongoing?)
Post-op Assessment - Cut (wound)
Surgical wound site – is dressing clean and dry and intact? If not, why not?
Drains? IV ABX? Bleeding? Incontinence?
Post-op Assessment - Exercise
Has the patient been up and mobilising?
Any walking aids?
What are routine post-op investigations on a joint replacement patient?
Bloods – FBC, U&E, (clotting?)
Check X-ray – any fractures caused by joint replacement surgery?
Any others relevant to PMH
Which joints are commonly affected by OA?
Commonly affects the hip, knee, DIP, PIP, thumb, CMJ, and hallux MTP joints.
Classically spares the MCPJs
OA - clinical features
Progressive pain
=> Initially activity related, then finally a constant rest pain
Stiffness
=> Characteristically worse after periods of rest (“gelling”), but lasts <30mins
Symptoms classically follow a waxing and waning course
Later features:
- Muscle wasting
- Loss of mobility
- Deformity
- Joint instability
OA - on examination
Look – bony swelling, muscle wasting
Feel – joint line tenderness, possible effusion, crepitus
Move – limited range of movement
RFs for OA
Age
Obesity
FHx
Gender (more common in women, particularly after menopause)
Hypermobility
Occupation (miners, farmers, etc.)
Secondary OA
Due to:
- Pre-existing joint damage – inflammatory / septic / crystal arthritis, AVN, trauma
- Metabolic disease – acromegaly, chondrocalcinosis, haemochromatosis
- Systemic disease – haemophilia (leading to haemarthroses), haemoglobinopathies, neuropathies
Hip OA
More common in males
Unilateral presentation
Generally does poorly and requires arthroplasty
O/E:
=> Painful, decreased internal and external rotation of the hip
=> Positive Trendelenburg test
Knee OA
Strong relationship with obesity
Other RFs = previous trauma, or soft knee tissue injuries.
Often bilateral
Most often leads to genu varus deformities due to medial disease.
O/E – classically moderate effusion, decreased ROM, crepitus and quadriceps wasting.
Types of OA
Generlised OA - nodal/ erosive/ crystal-associated
Hip OA
Knee OA
Nodal Generalised OA
Joints of the hands are affected one by one over many years.
=> DIPs affected much more than PIPs
First presenting with painful swelling and impairment of function.
Then inflammatory phase settles after months/years to leave painless bony swellings posterolaterally
=> Heberden’s (DIPs) and Bouchard’s (PIPs) nodes
OA of the CMC and MCP joints of the THUMB also occur, with bony swelling and fixed adduction leading to the classical “squared hand” in OA
=> Other MCPJs are generally spared.
There is generally also large joint involvement.
Erosive OA
Rare
characteristic cysts seen on XR and a poor prognosis.
Crystal-associated OA
Calcium pyrophosphate deposition in the cartilage leads to chondrocalcinosis (pseudogout).
This can be asymptomatic, or leads to signs/Sx or OA
Knees and wrists are most commonly affected.
Pathology of OA
In OA, wear and tear leads to splitting and erosion of the articular cartilage, leading to narrowing of the joint space.
There is associated inflammation, with thickening of the joint capsule and synovium and eventually capsular fibrosis.
The loss of cartilage is progressive, leading to constant friction of two naked bone surfaces.
Small cysts develop beneath this abnormal bone surface, and osteophytes form as irregular outgrowths of the peripheral unstressed cartilage.
As the joints become less mobile and less used, there may be secondary atrophy of the associated muscles.
What are the 4 cardinal changes of OA on a radiograph?
- L – loss of joint space
- O – Osteophytes
- S – Subchondral Sclerosis
- S – Subchondral cysts
OA - Ix
Bloods:
- CRP/ESR,
- RF & ANA to r/o other pathologies
XR – two views to confirm the presence of OA
CT/MRI if XR does not correlated with clinical picture.
OA - Principles of Mx
Early OA is managed conservatively
More severe symptoms leading to loss of function are managed surgically.
OA - Conservative Mx
Patient education
Weight loss
Physiotherapy – strength/stability/ROM exercises
Reduction of mechanical factors – e.g. cushioned footwear, walking aids
Splints for ankles/wrists
Analgesia
=> Paracetamol and topical NSAIDs = 1st line
=> Oral NSAIDs (+PPI) and topical capsaicin second line.
Intra-articular XR-guided corticosteroid injections
Use of intra-articular corticosteroid injections in OA
Usually XR-guided
Provide short-term relief if there is a painful joint effusion
Variable length of relief – usually <6 weeks
OA - Surgical Mx
Total replacement arthroplasty:
=> Common in the knee/hip
=> Delayed for longer in the knee due to poorer outcomes
One compartment arthroplasty:
=> Can occur in the knee if one side of the articular surface is diseased
Young patients may benefit from arthroscopy and joint washout, to delay definitive Mx for months/years
Arthrodesis (= the fusion of two or more bones in a joint) can be used for the ankle, spine or hand.
Realignment osteotomies are also sometimes performed (hip/knee)
What is complex regional pain syndrome?
= abnormal neuroinflammatory response to a traumatic event
Classically occurs post injury or surgery.
The key symptoms are allodynia and persistent pain in the area affected, out of proportion to the initial injury.
There is also stiffness and swelling along with abnormal hair/nail changes.
Complex Regional Pain Syndrome - Ix
Must attempt to r/o common causes of polyarthritis/muscle stiffness (e.g. polymyalgia rheumatica, RA, ankylosing spondylitis, fibromyalgia, viruses, connective tissue diseases, etc)
Bone scans demonstrate increased activity in the affected limb.
Complex Regional Pain Syndrome - Mx
Once it has happened – specialist Mx, involving the pain team, psychological support and physiotherapy.
The focus of Mx is on PREVENTION – adequate analgesia at the time of injury and early mobilisation post-fracture.
Who gets fibromyalgia?
Prevalence of 2-3% in the UK, but up to 7% in females over 70.
Affects F:M 10:1
Fibromyalgia - risk factors
Wide variety of life events associated with life distress (e.g. divorce, alcoholism in the family, traumatic injury, low income).
What is fibromyalgia
= DIAGNOSIS OF EXCLUSION
Despite intensive investigation, no structural/ inflammatory/ metabolic or endocrine abnormality has been identified.
It is thought to be due to sleep abnormalities and abnormal pain processing.
Fibromyalgia - non-restorative sleep
Fibromyalgia sufferers have reduced delta sleep (deep, non-REM sleep), distinct from sleep abnormalities seen in depression.
Deprivation of this delta sleep in normal volunteers produces the signs and symptoms of fibromyalgia.
Fibromyalgia - abnormal pain processing
Fibromyalgia sufferers have reduced pain tolerance at characteristic sites throughout the body.
This is evidenced by exaggerated skin flare reactions to substances such as capsaicin and frequent occurrence of allodynia.
Fibromyalgia - common Sx
• Multiple regional pain
• Marked fatigue
• Low affect, irritability, weepiness
• Poor concentration, forgetfulness
• Non-restorative sleep.
Fibromyalgia - Variable locomotor symptoms:
• Early morning stiffness
• Subjective swelling of fingers only
• Numbness/tingling of all fingers.
Fibromyalgia - Additional non-locomotor symptoms:
• Tension headache
• IBS
• irritable bladder
• Hyperacusis, dyspareunia, discomfort when touched (allodynia)
• Common side effects with drugs
• Chronic Fatigue Syndrome
Fibromyalgia - Diagnosis
- Take a thorough history – ruling out underlying pathology (red flags) and depression
- Bloods – may help to r/o underlying pathology
• FBC – anaemia
• ESR/CRP – inflammatory disease
• Consider RF/ANA if raised inflammatory markers
• TFTs – hypothyroidism
• Calcium, ALP – hyperPTH / osteomalacia
DIAGNOSTIC CRITERIA:
=> Widespread pain for more than three months
=> Pain elicited by digital pressure at 11 or more defined pressure points (out of 18; L+R side are separate points)
Fibromyalgia - Mx
- Patient Education = central to management
- Lifestyle Advice
- Low-dose amitryptilline (10-75mg nocte)
- Self-help strategies:
=> Cognitive behavioural approach, relaxation techniques and other “coping strategies” should be encouraged.
Patient Education and Lifestyle advice in fibromyalgia
Explain that the disease does not reflect inflammation or damage.
The model of a self-perpetuating cycle involving loss of sleep and pain is often readily accepted.
Sensible increases in activity level to help improve sleep and thus reduce symptoms.
=> Graded exercise therapy is a more formal approach
Low-dose amitryptilline in Fibromyalgia
Can be very effective, reducing the excessive transmission of pain signals and increasing restorative sleep.
Many people with fibromyalgia will be intolerant to even small doses of amitryptilline
Differential diagnoses for neck pain
- Trauma (incl. whiplash injury)
- Mechanical neck pain
- Cervical spondylitis
- Cervical myelopathy
- Ankylosing spondylitis
- Fibromyalgia
Whiplash Injury
Acceleration-deceleration forces applied to the neck
Usually occurs in a RTA, with a patient wearing a seatbelt being struck from behind.
Presentation:
=> Complex pattern with pain in the neck, shoulder and arm as well as headache, dizziness and memory loss.
Can take months to settle
Whiplash Injury - Ix
radiology only indicated for those with suspected bony injury.
Whiplash Injury - Mx
Can take months to settle => Provide reassurance to the patient that this is normal
Encourage early return to usual non-provocative, pre-accident activities and early mobilisation
Simple oral analgesics
Consider referral to physiotherapy
What is mechanical neck pain?
What are the causes?
= general neck pain that cannot be attributed to a specific issue
- Injury
- Sleeping in an awkward position
- Poor Posture
What is Brachial Neuralgia / Cervical Radiculopathy?
What can cause it?
Due to compression of the cervical nerve roots.
Usually caused by osteophytes in older patients
More rarely, acute cervical disc prolapse following minor trauma in younger patients
Cervical radiculopathy - presentation
- Aching pain in the neck, going down the arm.
- Progressing to a mild loss of grip strength
- Dermatomal sensory loss
- Occasional sudden sharp pains down the arm
Cervical radiculopathy - Ix
Confirm diagnosis with XR/MRI
Cervical radiculopathy - Mx
Refer to neurosurgery
What is Cervical Myelopathy?
What can cause it?
= compression of the cervical spinal cord.
Can be due to:
- Osteophytes
- Cervical disc degeneration
- Malignancy
Cervical Myelopathy - Presentation
Presents in older patients, initially with problems with fine motor control in the hands (e.g. can’t chop food).
There is a slowly developing spastic gait
Pain is not a predominant presenting feature.
Cervical Myelopathy - On Examination
UMN signs below the level of compression
LMN signs at the level of compression:
=> E.g. C5/6 lesion – wasting and fasciculation on the deltoids & biceps with a hypo-reflexive bicep reflex by hyper-reflexive tricep reflex and spastic leg with upgoing plantars.
Hoffman’s sign will be positive
What is a positive Hoffman’s sign?
“flicking” the distal phalanx leads to flexion of the other fingers (UMN sign)
Cervical Myelopathy - Mx
Confirm with XR/MRI
Refer to neurosurgery for conservative/surgical interventions
Approach to assessing a patient with back pain
- Rule out life-threatening visceral pathology (AAA, MI, Pancreatitis)
=> Observations, targeted abdominal and cardio-respiratory examination
=> ECG / bloods - Assess history for red flag symptoms that indicate more severe pathology (TUNAFISH)
- Examine for red flag symptoms that indicate more severe pathology
=> Saddle Anaesthesia (Cauda Equina)
=> Midline tenderness on palpation (Malignancy)
What are red flags in a back pain Hx?
- Age <20 or >55
- Constant or progressive pain (including pain at night)
- B symptoms
- Bladder/bowel symptoms
- History of TB/HIV/malignancy
- Pain in the thoracic spine
- History of significant trauma
What are red flags on examination of a back pain Pt?
Saddle Anaesthesia (Cauda Equina)
Midline tenderness on palpation (Malignancy)
What is simple mechanical back pain?
= 90% of back pain cases
A diagnosis can be reached when the clinician is satisfied there is no specific cause for the pain.
Simple mechanical back pain - presentation
Pain in lumbosacral region
20-55 years old
Pain came on suddenly when lifting
Pain classically varies with physical activity, posture, time
May be referred to buttocks/thighs
O/E – palpable muscular spasm, which can cause local pain/tenderness
Simple mechanical back pain - Mx
Simple analgesia
Advice to continue with normal activities plus physiotherapy exercises
Prognosis is good – 90% recover from the acute attack within 6 weeks
=> Reassess at 6 weeks if the pain has not resolved
Acute Lumbar Disc prolapse - pathophysiology
Generally occurs between age 20-40
The nucleus pulposus of the disc herniates into the spinal canal
Most commonly occurs at L4/5, or L5/S1
If the herniation is to the extent that it causes compression of one of the nerve roots, then radicular pain will occur.
If the herniation of the disc is central rather than lateral, this can cause cauda equina syndrome (a neurosurgical emergency)
Acute Lumbar Disc prolapse - presentation
Can be precipitated by lifting, or even something minor like a sneeze or triggering event unknown.
After which, patient is seized with pain and unable to straighten up.
=> The pain will be worse on coughing/straining.
=> Pain moves into the buttock within hours and into the leg within a day or two.
Radicular pain will be present:
=> Severe piercing/stabbing pains and paraesthesia in one leg due to compression of sciatic nerve root.
=> Rarely, this can affect both legs.
ALWAYS ask about bladder/bowel symptoms that may suggest cauda equina (e.g. retention/incontinence)
Acute Lumbar Disc prolapse - examination
Patient may walk with a flexed leg, or with obvious scoliosis.
On spinal examination there may be scoliosis and palpable muscle spasm
Straight leg raising to 30 degrees produces pain:
=> If positive raising the contralateral leg, suggests a very large lesion.
Femoral stretch test may be positive (pain in anterior thigh).
Neurological exam will show muscle weakness, some loss of sensation and diminished reflexes at the affected level.
Always examine to r/o cauda equina:
=> PR – no sensation, loss of anal tone
=> Palpate the bladder – signs of retention (this will be painless and can be confirmed with a post-void bladder scan)
=> Check sensation on saddle area.
What muscles are most commonly affected in Acute Lumbar Disc prolapse?
The most common muscles affected are extensor hallucis longus and tibialis anterior (L4; extension of great toe; dorsiflexion of foot).
Peroneus longus and brevis may also be affected (L4/5; foot eversion)
Gastrocnemius/soleus are affected in lower lesions (S1/2; plantar flexion).
Acute Lumbar Disc prolapse - Ix and Mx
Thorough history to separate referred pain in simple lower back pain from “true” nerve root pain.
=> The natural history of disease is relapsing and remitting episodes of pain.
Examination - red flags?
Initial Mx = conservative:
- Anti-inflammatories and bed rest with knees slightly flexed.
- Bed rest for two weeks reduces herniation in more than 90%
- Rehabilitation with the physio is a vital part of Mx.
If symptoms persist at 2 weeks:
- Epidural injections are useful to treat radicular symptoms, these can be repeated fairly frequently
- MRI & surgical referral is indicated
- For single level disease, microdiscectomy may be performed (removal of the herniating material).
Cauda Equina Syndrome
- presentation
- Ix
- Mx
RARE (occurs in ~2% of disc prolapses) BUT EMERGENCY
Presentation = pain as per disc prolapse, PLUS bladder/bowel symptoms, saddle anaesthesia
Ix = Emergency MRI
Mx = Urgent surgical intervention required to prevent long-term bladder/bowel/reproductive problems.
What is Lumbar Canal Stenosis?
What can cause it?
Stenosis of the lumbar canal compresses the cauda equina roots, leading to symptoms of spinal claudication
Generally caused by degeneration of the spine.
- Facet joint hypertrophy
- Ligamentum flavum hypertrophy
- Disc degeneration
- OA
Lumbar Canal Stenosis - presentation
Sx of spinal claudication
=> Aching pain in the legs on walking, most commonly posteriorly.
=> Pain recovers fairly slowly on sitting/bending forwards (this creates a more spacious canal).
=> There may also be numbness, stiffness and weakness in the leg.
=> Symptoms are variable day to day.
This can have a stable or progressive course (which can influence choice of Tx )
Lumbar Canal Stenosis - Mx
Sx can have a stable or progressive course (which can influence choice of Tx – i.e. conservative vs surgical)
=> Conservative = activity modification, physiotherapy
=> Surgical = laminectomy
What is Spondylolithesis?
Facet joints are responsible for keeping vertebrae in antero-posterior alignment.
In spondylolisthesis, one vertebra is displaced (either anteriorly or posteriorly) on the vertebra below it – anterolisthesis or posterolisthesis
Almost always occurs between L4-L5 or L5-S1
At which levels does Spondylolithesis most commonly occur?
Almost always occurs between L4-L5 or L5-S1
What causes spondylolithesis?
Spondylolysis = most common cause; stress fracture of lumbar pars articularis.
Dysplasia of the lumbosacral facet joints (in adolescents)
OA of the facet joints
In extreme athletes
Spondylolithesis - Presentation
Intermittent back ache, precipitated by exercise/strain
O/E – often can find a “step”
Cauda equina syndrome can develop
Spondylolithesis - Mx
Usually managed conservatively – as per mechanical back pain.
Spinal fusion can be performed if the patient is young or there are disabling symptoms
Facet joint Dysfunction
= Highly common cause of lower back pain presenting to the GP.
Causes:
- The facet joints are synovial, so can develop OA/RA.
- More commonly the joints are affected by minor trauma.
Presentation of Facet Joint Dysfunction
Can lead to acute or chronic back pain
Typically worse on extension of the back, in the morning and on standing.
NO history of pain in the legs
OE – there may be local tenderness over the facet joints
Non-mechanical causes of Back Pain
Inflammatory (spondyloarthropathies)
Infection (discitis)
Metabolic (wedge fractures)
Neoplastic (primary or secondary)
Discitis
- cause
- presentation
- management
can present as a complication of spinal surgery/injections.
Localised pain and raised inflammatory markers
Admit Pt for IV ABX
Neoplastic causes of back pain
What are typical symptoms?
Can be primary tumours, or most commonly secondary metastases (BLT KP)
Sx = progressive pain, particularly at night with no exacerbating/relieving factors; there may be pain over a particular bony segment.
Who is more likely to get RA?
Pre-menopausal women are affected more than men, but there are no gender differences post-menopause.
Classic presentation is in a 30-50 year old woman
RA - Presentation
Classically presents as a symmetrical polyarthritis
=> Typically in a 30-50 year old female.
Red, warm, painful & swollen peripheral joints (typically of the hands and feet)
This then progresses to larger joints (still symmetrical)
Symptoms worse in the morning
Tends to evolve over weeks/months (but in 15% of cases there is rapid onset of Sx over days/overnight.)
General malaise, weight loss and disturbed sleep are common
Extra-articular features may be present
What are some rarer presentations of RA?
• Palindromic RA (recurring mono/polyarthritis)
• Persistent monoarthritis
• Systemic illness with extra-articular symptoms
RA - Hand involvement
Involvement of the small joints of the hands is most common, with joint erosion leading to deformities as the disease progresses.
=> DIPJs are classically spared in RA
There are certain characteristic deformities:
- Ulnar deviation at the MCPJs
- Radial deviation at the wrist
- Boutonniere deformity
- Swan neck deformity
- Z-deformity of the thumb –
- Subluxation is a late deformity – volar subluxation at the MCPs/wrist
Severe disease can lead to ankylosis (fusion) across the joint, leading to severe and fixed deformities.
Carpal tunnel syndrome is also very common due to inflamed tendon sheaths.
Boutonniere deformity
= hyperflexed PIPJs, hyperextended DIPJs
Swan neck deformity
= hyperflexed DIPJs, hyperextended PIPJs
Z-deformity of the thumb
= flexed MCPJs, extension at IPJ
What are the characteristic hand deformities of RA?
- Ulnar deviation at the MCPJs
- Radial deviation at the wrist
- Boutonniere deformity
- Swan neck deformity
- Z-deformity of the thumb
- Subluxation is a late deformity – volar subluxation at the MCPs/wrist
RA - Foot involvement
MTPJ swelling is one of the earliest manifestations.
The foot becomes broader and hammer-toe deformity develops
Ulcers/callouses can occur due to exposure of the metatarsal heads to pressure, due to migration of the protective fat pad.
RA - large joint involvement
The knee is most commonly affected, then the shoulder/hip.
RA - large joint involvement
The knee is most commonly affected, then the shoulder/hip.
In the knee, genu valgus deformity and secondary OA can develop.
Once severely affected, large joints require total joint replacement to restore function.
RA - Ix
History & Examination
Bloods - FBC, CRP/ESR, RF, Anti-CCP, ANA
X-Ray
What bloods might be done for RA?
• FBC – leucocytosis & thrombocytosis in acute inflammatory phase; normocytic anaemic of chronic disease.
• CRP/ESR – elevated in active disease
• Rheumatoid Factor (RF) – elevation in 70%, but non-specific.
• Anti-CCP – more specific, rises predate clinical disease by several years.
• Anti-nuclear Antibody – if suspecting connective tissue disease
X-ray findings in RA
Early findings – soft tissue swellings around the PIPJs and MCPJs
=> DIPJs usually spared
L – loss of joint space (uniform joint space narrowing)
E – erosions
S – Soft tissue swellings
S – soft bones (osteopaenia)
Subluxation/ dislocation may also be seen
Which joints are typically spared in RA?
the DIPJs
Pathogenesis of RA
- First change = rheumatoid synovitis
=> Swollen synovium showing a villous pattern and neutrophil infiltration. - This leads to an exudative effusion within the joint.
=> Presents clinically as a boggy, swollen joint. - As the disease progresses, vascular granulation tissue grows from the peripheries inwards, destroying articular cartilage.
=> Also causes focal destruction of the bone, causing “erosions” seen on radiographs.
=> Clinically this can lead to deformities. - In long-standing disease, the whole cartilage may be destroyed and replaced by fibrous pannus, leading to secondary OA changes.
What is the most likely cause of morning stiffness in RA?
thought to be either due to the cortisol trough, or the build-up of inflammatory mediators during non-activity.
Rheumatoid Nodules
Seen in 20% of patients with RA.
Formed of necrotic inflammatory tissue
Occur over bony prominences at sites of recurrent mechanical stress
=> E.g. the olecranon, calcaneum and MCP joints
Associated with underlying erosions
Vary in size from a few mm to cm in diameter
More common in smokers
ONLY occur in seropositive disease
Extra-articular Rheumatoid Disease
RHEUMATOID NODULES
PULMONARY - pulmonary fibrosis, pleural effusions
VASCULITIS - cutaneous, mesenteric, etc.
CARDIAC - subclinical pericardial involvement; higher rates of atherosclerosis
NERVOUS SYSTEM -
• Entrapment neuropathies such as carpal tunnel are common.
• Glove & stocking sensory loss can also occur due to vasculitis of the vasa nervorum.
EYES
• Keratoconjunctivitis sicca
• Scleritis and episcleritis
KIDNEYS - amylodoisis => renal failure
HAEMATOLOGY
• Felty’s Syndrome = splenomegaly + anaemia + neutropaenia associated with RA
• Normocytic chormochromic anaemia.
What is Felty’s Syndrome?
Felty’s Syndrome = splenomegaly + anaemia + neutropaenia associated with RA
What is atlantoaxial instability / subluxation?
In whom does it occur?
= is radiologically identified increased mobility or laxity between the body of the first cervical vertebra (atlas) and the odontoid process of the second cervical vertebra (axis).
It occurs in 50-80% of patients with RA of the cervical spine, as the transverse and apical ligaments are destroyed by pannus.
atlantoaxial instability - presentation
Localised pain & deformity
Cervical radiculopathy
Atlantoaxial instability - Ix and Mx
Investigations:
- XR – APO, lateral and odontoid peg views required
- MRI of the cervical spine
Management:
- Surgical decompression of the spinal cord
- Stabilise involved segment of the spine.
RA - Management
Once diagnosis is confirmed:
- Methotrexate is 1st line, usually combined with hydroxychloroquine (as they have different side effect profiles).
- Short-term glucocorticoids (IM methylprednisolone) are also prescribed at diagnosis to reduce inflammation before the DMARDs become effective.
=> Further short-term glucocorticoid courses may be required to deal with flares. - NSAIDs are often also essential in a patient’s management to relieve night pain and morning stiffness.
- Lifestyle measures are also very important
=> Stopping smoking, hydrotherapy, etc. - MDT management is essential
Why is stopping smoking important for RA patients?
Reduces CV risk and increases DMARD effectiveness
Who is affected by gout?
The prevalence of gout is ~1%.
There is a strong male predominance (10:1)
=> the most common inflammatory arthritis in men over 40.
Pathophysiology of gout
A pathological reaction of the joint/periarticular tissues due to presence of monosodium urate monohydrate (MSUM) crystals.
These preferentially deposit in the peripheral connective tissues in and around synovial joints, initially favouring the lower limb.
=> It will classically first present in the 1st MTP joint.
As the crystal deposits slowly increase, there is progressive involvement of more proximal sites, and the potential for development of secondary OA.
Does hyperuricaemia cause gout?
Hyperuricaemia is not alone sufficient to cause gout
=> 95% of hyperuricemic people never develop gout.
ALSO a normal uric acid level during an acute attack does not exclude gout (levels fall as part of the acute reaction).
Gout - RFs / Causes
• Hyperuricaemia
• Age
• Metabolic syndrome
• High protein diet
• High alcohol intake (predominantly beer)
Secondary Causes of Gout:
1. Factors that impair excretion of uric acid
=> e.g CKD, drugs (NSAIDs, thiazides), HTN, HyperPTH, hypothyroidism
- Factors that increase production of uric acid:
=> e.g. Metabolic conditions, myelo-/lympho- proliferative disorders
Acute Urate Gout - Presentation
Severe pain, often described as the “worst ever”
Rapid onset of symptoms, often waking the patient
Maximum severity reached in 2-6 hours
Associated extreme tenderness (patient unable to wear a sock) and marked swelling and erythema.
There may be accompanying malaise, fever or confusion (more common if large joint affected).
The joint will be held in the “loose pack” position.
“Loose-packed” position of joint
= a position of a joint in which the joint surfaces are not congruent and the joint capsule is lax.
What can precipitate a gout attack?
may be precipitated by excess food/alcohol or dehydration.
How long does a gout attack last?
It is generally self-limiting over 5-14 days with a complete return to normality (although desquamation of overlying skin is common).
How does septic arthritis compare to gout?
main DDx of gout = septic arthritis
Septic arthritis = more subacute onset, progressing in severity until treated, ROM will be limited, systemic Sx.
Tophaceous Gout
Large MSUM crystal deposits produce irregular, firm nodules (“tophi”) at classical sites.
Usually located at extensor surfaces of fingers, hands, elbows, and Achilles tendon
The white colour may allow distinction from rheumatoid nodules.
Large nodules may ulcerate, discharging white, gritty material and associated with local inflammation.
Gout - Ix
Bloods:
=> FBC, U&E, serum urid acid.
Aspiration of the joint effusions
=> For MCS and polarised light microscopy
X-Ray:
=> Can assess the degree of joint damage
In the longer-term, it may be relevant to search for an underlying cause – e.g. BP, urine dip, blood glucose/lipids, and FBC/ESR performed during remission.
Acute Gout Attack - Mx
Fast-acting oral NSAID (e.g. naproxen / diclofenac)
Oral Colchicine is used instead of NSAIDs in certain patients
=> e.g. Renal patients, patients with CCF, patients on chemotherapy
Early aspiration of the joint combined with corticosteroid injection can effectively abort the acute attack
= Only really in secondary care with immediate microscopy.
EARLY MOBILISATION is important after an episode of gout.
Long-term Management of Gout
LIFESTYLE ADVICE:
- Reduce alcohol and total calorie/cholesterol intake; maintain a healthy weight.
- Avoid some foods that are high in purines (offal, seafood, red meat, asparagus, spinach) / smaller portions of these.
ALLOPURINOL
=> reduces uric acid production
