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
Indications for use of hypouricaemic drugs in long-term management of gout
- Recurrent attacks of gout
- Tophaceous gout
- Evidence of bone/joint damage
- Associated renal disease
- Greatly elevated uric acid levels
Use of Allopurinol for gout
Tx with allopurinol is only initiated when an acute attack has settled (usually after 4 weeks), so as not to exacerbate/prolong the attack.
The aim of Tx is to bring serum uric acid level into the lower half of normal range.
=> The serum level should be measured every month, and the dose increased in 100mg increments, to maximum of 900mg daily, until uric acids are within this range.
After this, monitoring can move to yearly.
What findings might there be on joint aspiration of a joint with gout?
In acute gout, synovial fluid shows increased turbidity due to the elevated cell count.
Urate crystals will be negatively birefringent and needle shaped in polarised light microscopy
What is pseudogout?
Calcium pyrophosphate crystal deposition in hyaline/fibrocartilage of joints leads to chondrocalcinosis
Causes and RFs of pseudogout
May be sporadic, familial or associated with metabolic diseases:
=> HyperPTH, hypophosphatasia, hypomagnesaemia, Wilson’s disease.
- Associated with aging
- More common in women
Pseudogout - presentation
Often asymptomatic
can present as an acute self-limited synovitis (pseudogout) or chronic arthritis showing a strong overlap with OA.
Typically occurs at the knee or wrist
Typically in elderly women.
O/E – signs of OA with superimposed synovitis.
Pseudogout - Ix
= AS PER GOUT Ix
Bloods
Polarised light microscopy of joint aspirate will show positively bifringent, rhomboid shaped crystals.
XR may show chondrocalcinosis
Pseudogout - Mx
Acutely is treated very similarly to gout
Often responds well to joint aspiration
Calcific periarthritis
= acute juxta-articular soft tissue deposition of calcium hydroxyapatite crystals leading to an acute inflammatory response.
=> Periarticular tissues – particularly tendons, causing calcific tendonitis
=> Hyaline cartilage (in association with OA; will make OA more severe)
=> S.c. Tissue / muscle – in connective tissue diseases
ASIA Index/Exam
= a scoring system that helps to determine whether a spinal cord injury is complete or incomplete.
Myotome and dermatome function are recorded in the upper/lower limb.
Preservation of any myotome/dermatome function in S4/5 represents an incomplete spinal cord injury, with potential for recovery.
=> E.g. anal tone, or feeling of pressure
Barthel Index
= a scale used to assess a patient’s performance in 10 functions/ADLs
A higher score = a reflection of greater ability to function independently following hospital discharge.
What 10 aspects are assessed in a typical Barthel Index?
- Bladder continence
- Bowel continence
- Grooming
- Toilet use
- Feeding
- Transfer
- Mobility
- Dressing
- Stairs
- Bathing
What is considered a joint dislocation?
A dislocation occurs when the joint surfaces are completely displaced and no longer in contact
Joint Dislocation - Ix
History
Examination:
=> obvious deformity, with displaced bony landmarks.
=> Other neurovascular features/injuries should be checked for in these patients (always check for neurological deficiencies prior to reduction).
Ix = XR is normally the investigation of choice.
Joint Dislocation - Mx
= urgent joint reduction to maintain vascularity of the joint
stabilisation of any associated fractures.
What is the most common direction of shoulder dislocation?
90% being anterior dislocations.
=> Often due to FOOSH or occasionally direct trauma.
What is the rarer direction of shoulder dislocation?
What is the typical sign for this?
Posterior dislocations are rarer
Seen in direct trauma to the front of the shoulder, or patients who have had a seizure (or been electrocuted).
=> Classical “lightbulb” sign on XR
What nerve in particular should be tested in shoulder dislocation?
The axillary nerve should be tested before and after reduction, as it is commonly injured
=> Provides dermatomal sensation to the “regimental badge” area of the shoulder.
What is charcot foot?
= a rapidly progressing destructive process, occurring in the foot/ankle joints in people with peripheral neuropathy.
Charcot Foot - O/E
EARLY STAGES – local oedema, and warmth
LATER STAGES – obvious deformities
=> “rocker bottom” foot if midfoot affected
=> Toes can curl under (like claws)
=> Heel deformities
Charcot Foot - causes
DM = most common
Tabes Dorsalis (syphilitic myelopathy)
Alcoholic neuropathy
Cauda equina lesions
Leprosy
Charcot Foot - Ix
X-RAY
- Can be normal initially
- Then shows initial local osteoporosis
- Progresses to show osseus destruction and collapse.
Charcot Foot - Mx
Well-fitting cast to prevent weight-bearing in early stages.
=> Until the redness, swelling, and heat are resolved.
Then prescription footwear
Surgical Mx of severe deformities.
Neurogenic Bladder
Bladder dysfunction due to neurological damage.
Can present with a range of symptoms
=> Injury above T12 usually leads to a reflex bladder
=> Injury below L1 usually leads to a flaccid (acontractile) bladder
“Reflex bladder”
Usually due to injury above T12
Autonomic control but no voluntary control – the bladder contracts when reaching a certain level of fullness
Mx = regular “tapping” (tapping the suprapubic area with the side of the hand to stimulate the autonomic reflex) or intermittent catheterisation.
“Areflexic Bladder”
Usually due to injury below L1 leads to a flaccid (acontractile) bladder
=> there is no bladder tone, so looks clinically like overflow incontinence.
Mx = intermittent self catheterisation.
Neurogenic Bowel - causes and Mx
= bowel dysfunction due to neurological damage
=> Spinal Cord Injury above T12 leads to reflex bowel.
=> Injury below L1 leads to areflexic bowel.
Mx:
- Keeping the correct stool consistency
- Routine defecation at set times of day (triggered by enema, digital stimulation, postural changes or abdominal massage).
“Reflex Bowel”
Usually due to spinal Cord Injury above T12
The feeling of rectal fullness is lost
Reflex bowel movements cause emptying at inconvenient times
“Areflexic Bowel”
Usually due to injury below L1
Defecation reflex and anal sphincter contraction is lost.
What is Autonomic Dysreflexia?
What can cause it?
= a potentially dangerous clinical syndrome that develops in individuals with spinal cord injury at T6 or above.
=> Results in acute, uncontrolled HTN due to sympathetic overactivity.
Can be precipitated by any noxious stimulus below the level of the injury (e.g. full bladder/bowel, skin irritation, sexual activity or minor trauma).
Autonomic Dysreflexia - Presentation
a clinical emergency in individuals with spinal cord injury
Sx:
- Pounding headache
- Sweating
- Blotching of the skin above the injury, with cold & clammy skin below.
O/E:
- HTN (above 200/100) and bradycardia.
What is Septic Arthritis?
= infection of a joint
SURGICAL EMERGENCY - mortality rate of 10% and high morbidity (infection is rapidly destructive of joint)
Causes of septic arthritis
Patients with septic arthritis invariably also have a bacteraemia, as spread is generally haematogenous (most commonly from the skin/respiratory tract).
Direct infection following joint aspiration is uncommon.
Septic Arthritis - RFs
- Extremes of age
- Pre-existing joint disease (principally RA)
- IVDU
- DM / immunosuppression
- Recent operative / injective procedures on the joints
Septic Arthritis - causative organisms
Most likely causative organism = Staph. aureus,
In young adults, disseminated gonococcal infection is an important cause.
In children, Strep. pneumoniae or H. influenzae may be the causative organism in children.
Septic Arthritis - presentation
Acute/subacute monoarthritis – a hot, swollen, erythematous joint.
The joint is held in the “loose pack” position (e.g. knee flexed)
O/E:
- Fever and systemic Sx
- Demonstratable effusion
- Loss of movement of the joint
- Extreme pain with even passive movement.
The knee/hip joints are most commonly affected.
DDx of septic arthritis
crystal arthritis,
osteomyelitis,
reactive arthritis,
overlying cellulitis,
monoarticular presentation of RA/CTD/seronegative arthritis.
Septic Arthritis - pathophysiology
The joint is invaded by haematological spread, by eruption of a bone abscess or directly through a penetrating wound.
Infection spreads through the joint and cartilage is destroyed.
Pus bursts out of the joint to form abscesses and sinuses.
With healing, the raw articular surfaces may adhere to produce ankylosis.
Septic Arthritis - Ix
Joint Aspiration = essential first step
=> For gram stain and culture
=> Aspirated fluid may look normal, or can often be turbid/blood-stained.
If the joint is not readily accessible (e.g. hip, spine, SIJ) aspiration should be performed in theatre under image guidance.
Blood Cultures:
=> Ensure sample has been received by the lab before commencing ABX
Other bloods – FBC, ESR/CRP, uric acid, clotting.
(Imaging - XR of no value in acute phase )
Appearance of septic arthritis on imaging
X-rays are of no value in the acute diagnosis of septic arthritis, but there are characteristic changes related to the disease pathophysiology.
Soft tissue swelling in the first two weeks, with widening of joint space due to effusion.
Later X-rays will then show narrowed joint space as the cartilage is destroyed, with signs of bone destruction and finally ankylosis if severe.
Septic Arthritis - Mx
- A to E Resuscitation and Sepsis 6
- Admission under orthopaedics
- Once the joint has been aspirated and blood cultures taken, start Empirical IV ABX
- Adequate pain relief
- Early source control with in-theatre washout
- Early active rehabilitation improves outcomes.
IV ABX is usually continued for 2-3 weeks, followed by 6 weeks of oral Tx
=> Duration of Tx is guided by CRP/ESR monitoring
How long are ABX usually continued in treatment of septic arthritis?
IV ABX is usually continued for 2-3 weeks, followed by 6 weeks of oral Tx
=> Duration of Tx is guided by CRP/ESR monitoring
What is osteomyelitis?
What are common sites?
Osteomyelitis = infection of the bone.
Common target sites for acute infection are:
- the long bones in children
- the vertebrae in immunosuppressed adults.
Chronic infection in adults or children can occur following open fractures or operative procedures.
Osteomyelitis - RFs and causative organisms
generally carries the same risk factors and organisms as septic arthritis.
Osteomyelitis - presentation
Usually in a child
Continuous pain, often throbbing and worse at night.
Fever and general malaise
Local swelling, erythema, warmth and oedema (late signs)
May be unable to weight-bear
Osteomyelitis - pathophysiology
- Inflammation – acute inflammatory response, leading to increased intraosseous pressure and intense pain.
- Suppuration – pus appears in the medulla (day 2) and forces its way to the surface to form a subperiosteal abscess, which can form a sinus to drain to the surface or drain into soft tissues/joints.
- Necrosis – compromised blood supply leads to necrosis by day 7.
- New bone formation – osteoblasts stimulate new bone formation.
- Resolution – bone will eventually heal (although remain thickened) with ABX and controlled intraosseous pressure.
Osteomyelitis - Ix
X-rays often do not show any changes, particularly in early disease.
=> They cannot be used to exclude osteomyelitis.
MRI = best imaging for establishing a diagnosis.
Bloods – FBC, CRP/ESR
=> Will show raised inflammatory markers
Blood cultures may be positive for the causative organism.
Bone cultures from bone biopsy at debridement = gold standard
What are the potential signs of osteomyelitis on X-ray?
MOST OFTEN NO CHANGES
The potential signs of osteomyelitis on an x-ray are:
• Periosteal reaction/ thickening (changes to the surface of the bone)
• Localised osteopenia (thinning of the bone)
• Destruction of areas of the bone, endosteal scalloping
What is the best imaging for establishing a diagnosis of osteomyelitis?
MRI
What is gold-standard for diagnosing osteomyelitis?
Bone cultures from bone biopsy at debridement
=> can establish the causative organism and the antibiotic sensitivities.
Osteomyelitis - Mx
Mx involves a combination of surgical debridement and antibiotic therapy.
ABX:
- 6 weeks of flucloxacillin +/- rifampicin or fusidic acid added for the first 2 weeks
(Alternatives to flucloxacillin are clindamycin in allergy or vancomycin or teicoplanin for MRSA)
SURGERY:
Osteomyelitis associated with prosthetic joints may require complete revision surgery to replace it
Curretage of the area may be required if:
- the patient clinically deteriorates,
- the limb shows evidence of deterioration,
- imaging shows progressive bone destruction,
Viral arthropathy
Viral arthralgia can be caused by basically any viral infection.
It tends to occur during the prodromal phase, along with a viral rash.
It tends to be symmetrical and is NON-DESTRUCTIVE so does not lead to any form of chronic disease.
Neck pain - DDx
- Trauma (incl. whiplash injury)
- Mechanical neck pain
- Cervical spondylitis
- Cervical myelopathy
- Ankylosing spondylitis
- Fibromyalgia
Whiplash Injury - Cause and presentation
Acceleration-deceleration forces applied to the neck
=> Usually occurs in a RTA, with a patient wearing a seatbelt being struck from behind.
Presentation:
- Pain in the neck, shoulder and arm - as well as headache, dizziness and memory loss.
Whiplash Injury - Ix and Mx
Ix – radiology only indicated for those with suspected bony injury.
Can take months to settle
=> patient education, analgesia, try to move as normal
Causes of mechanical neck pain
- Injury
- Sleeping in an awkward position
- Prolonged keyboard working.
Mechanical Neck Pain - Presentation
Pain is associated with palpable muscle spasm
Can radiate up to the occiput and can be associated with tension headache.
What is Cervical Radiculopathy?
Also known as brachial neuralgia
= Pain 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 and Mx
Ix:
= Confirm diagnosis with XR/MRI
Mx:
= Refer to neurosurgery
What is cervical Myelopathy?
What can cause it?
= compression of the cervical spinal cord.
Causes:
- Osteophytes
- Cervical disc degeneration
- Malignancy
Cervical Myelopathy - Sx
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 - O/E
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 but hyper-reflexive tricep reflex and spastic leg with upgoing plantars.
Hoffman’s sign will be positive:
=> “flicking” the distal phalanx leads to flexion of the other fingers (UMN sign)
What is a positive Hoffman’s sign?
“flicking” the distal phalanx leads to flexion of the other fingers (UMN sign)
Cervical Myelopathy - Ix and Mx
Confirm with XR/MRI
Refer to neurosurgery for conservative/surgical interventions.
RED FLAG back pain symptoms
History:
T – trauma
U – unexplained weight loss (and other B symptoms)
N – Neurological symptoms
A – Age >50 or <20
F – Fever
I – IVDU
S – steroid use
H – History of cancer
O/E:
=> Saddle Anaesthesia (Cauda Equina)
=> Midline tenderness on palpation (Malignancy)
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 - Ix and Mx
A diagnosis of non-specific lower back pain can be reached when the clinician is satisfied there is no specific cause for the pain.
Mx:
- Simple analgesia
- Advice to continue with normal activities plus physiotherapy exercises
=> Reassess at 6 weeks if the pain has not resolved.
Acute Lumbar Disc Prolapse
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
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 - O/E
- there may be scoliosis and palpable muscle spasm
- Straight leg raising produces pain
- 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 should be done if ?Cauda Equina
Emergency MRI and urgent surgical intervention required to prevent long-term bladder/bowel/reproductive problems.
What is Lumbar Canal Stenosis?
What causes 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
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.
Spondylolisthesis
= when one vertebra is displaced (either anteriorly or posteriorly) on the vertebra below it => anterolisthesis or posterolisthesis
Almost always occurs between L4 and L5 or L5 and S1.
Spondylolisthesis - Presentation
Intermittent back ache, precipitated by exercise/strain
O/E – often can find a “step”
Cauda equina syndrome can develop
Spondylolisthesis - Causes
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
Spondylolisthesis - 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 - causes
The facet joints are synovial, so can develop OA/RA.
More commonly the joints are affected by minor trauma.
Facet Joint Dysfunction - Presentation
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
What is classed as “non-mechanical” back pain?
inflammatory (spondyloarthropathies)
infective (discitis)
metabolic (osteoporosis)
neoplastic (1o or 2o)
Discitis - causes, presentation, Mx?
Discitis can present as a complication of spinal surgery/injections.
Localised pain and raised inflammatory markers
Admit Pt for IV ABX
Wedge Fracture - Presentation
May be asymptomatic, or cause localised pain (can radiate around the ribs).
Multiple fractures lead to increased thoracic kyphosis.
XR shows wedging and loss of anterior vertebral body height.
Sx of neoplastic back pain
= progressive pain, particularly at night with no exacerbating/relieving factors;
There may be tenderness over a particular bony segment
Link between PMR and GCA
both are types of large vessel vasculitis
15-30% of patients with PMR will develop GCA
50-70% of patients with GCA will develop PMR
Polymyalgia Rheumatica - Presentation
Patient always >50
Sudden onset, severe pain and stiffness in the shoulders, neck, hips and lumbar spine.
Worse in the morning, lasting for over 30 minutes.
Systemic features of tiredness, fever and weight loss.
Polymyalgia Rheumatica - O/E
muscles may be tender to palpate, especially in the upper arm (e.g. when measuring BP)
Diagnosis of polymyalgia rheumatica
Symptoms of bilateral shoulder/pelvic girdle aching alongside morning stiffness and evidence of an acute phase response must be present for over 2 weeks for diagnosis to be made.
After a diagnosis has been made, it is essential to assess for GCA
GCA - Presentation
- Severe headaches
- Scalp (when combing hair) or temporal tenderness
- Jaw claudication whilst eating.
If untreated, there will be sudden painless loss of vision due to ischaemia of the optic nerve.
GCA - OE
may be tenderness/swelling of one or both temporal arteries; the overlying scalp may be inflamed.
PMR/GCA - Ix
- Normocytic, normochromic anaemia
- Raised ESR/CRP
- Often raised ALP/GGT on LFTs
- RF/ANA/anti-CCP negative
- CK negative
- MRI/USS will show evidence of peri-articular inflammation (bursitis/tenosynovitis) in PMR
If there are features of GCA, a TEMPORAL BIOPSY should also be taken as a definitive diagnostic test (although often not performed in practice).
GCA - temporal biopsy
= the definitive diagnostic test
=> Intimal hypertrophy, with giant cells and inflammatory infiltrate
Skip lesions occur, so negative biopsy does not exclude the diagnosis.
PMR - Mx
Oral Prednisolone – high dose initially to prevent GCA developing
15mg o.d.
Response to steroids is usually rapid – consider alternative diagnosis if there is no response within 48 hours.
Dose reduction occurs over a long time in line with disease response (determined by regular ESR/CRP levels).
=> Most PMR patients require treatment for 2 years
Always prescribe bone protection and PPIs!!!!
GCA - Mx
Oral Prednisolone – high dose initially to reduce the risk of permanent optic damage
60mg o.d. if visual symptoms,
40mg o.d. if no visual symptoms
Response to steroids is usually rapid – consider alternative diagnosis if there is no response within 48 hours.
Dose reduction occurs over a long time in line with disease response (determined by regular ESR/CRP levels).
=> Most GCA patients require treatment for up to 5 years
Always prescribe bone protection and PPIs!!!!
What should be done if a ?GCA patient has visual symptoms?
Same day referral to ophthalmology
Primary Sjogren’s
= dry eyes (keratoconjunctivitis sicca) in the absence of any autoimmune disease.
Secondary Sjogren’s
= presence of sicca symptoms, in the presence of autoimmune disease.
=> Most commonly RA, but also SLE, scleroderma and polymyositis.
What is Sjogren’s syndrome?
Who does it affect?
= a long-term disease that affects the body’s moisture-producing (lacrimal and salivary) glands.
Affects F:M – 10:1
Can affect anyone, but most commonly women during middle age or after menopause.
Sjogren’s Syndrome - Sx
• Fatigue
• Dry eyes and mouth
• Salivary and parotid gland enlargement
• Vaginal dryness
Associated systemic features:
- Arthralgia
- Raynaud’s
- Oesophageal motility issues
Sjogren’s Syndrome - Ix
Schirmer’s Tear Test
- <5mm = dry eyes.
- >15 mm = normal
- 5-15 mm = grey area
Bloods:
- RF usually raised
- ANA – raised in 70%
- Anti-Ro – positive in 70%
- Anti-La – positive in 30%
How is Schirmer’s Tear Test performed?
Specialised filter paper placed inside lower eyelid and the eyes are closed
The strip of paper will absorb any tears and indicate the volume of water present.
Distance checked after 5 mins
<5mm = dry eyes.
5-15 mm = grey area
>15 mm = normal
Sjogren’s Syndrome - Mx
Patient Education
Avoid prolonged screen use
Reduce smoking & alcohol, avoid smoky/dry environments
Maintain good oral hygiene
Analgesia for pain
Artificial Tears & Saliva & vaginal lubricants
Mx of any underlying condition (e.g. SLE, scleroderma, etc).
Hydroxychloroquine to halt progression of the disease
What do Sjogren’s patients need monitoring for?
Need close monitoring for risk factors and development of non-Hodgkin B cell lymphoma
=> 1 in 6 patients will develop this
What systemic symptoms could suggest vasculitis?
GENERAL – malaise, fever, weight loss, myalgia, arthralgia
SKIN – palpable purpura, ulceration
GI – mouth ulcers, abdominal pain, diarrhoea
RESP – haemoptysis, dyspnoea
ENT – epistaxis, crusting
CARDIAC– chest pain
NEURO - Neuropathies
What can cause vasculitic conditons?
can be primary,
or secondary to malignancy/ infection/ connective tissue diseases
Vasculitis affecting large vessels
GCA
Takayasu’s arteritis
Vasculitis affecting medium vessels
Classic Polyarteritis Nodosa
Kawasaki Disease
Vasculitis affecting medium/small vessels
Granulomatosis with Polyangiitis (Wegener’s Granulomatosis)
Churg-strauss Syndrome
Microscopic Polyangiitis
Vasculitis affecting small vessels
HSP
Cryoglobulinaemia
Takayasu’s arteritis
= vasculitis of large vessels (typically the aorta and its main branches)
Typically affects young adults of Asian descent
Presents with:
- Pulseless upper limbs
- Upper limb claudication
- Stroke
Classic Polyarteritis Nodosa
= vasculitis affecting medium-sized muscular arteries
Multi-systemic symptoms
Sometimes associated with HepB/C infection
Kawasaki Disease
= medium vessel vasculitis
Fever, rash, lymphadenopathy and palmar erythema in children.
Can affect the coronary arteries.
Wegener’s Granulomatosis / Granulomatosis with Polyangiitis
= vasculitis of medium/small vessels
Commonly affects the lung, kidney, and ENT systems
- Mouth ulcers,
- saddle nose,
- proptosis,
- Lung granulomas (=> erosive, causing haemoptysis),
- petechial haemorrhages.
Granuloma formation seen on biopsies, granulomas are very invasive
Churg-strauss Syndrome
= vasculitis of medium/small vessels
Associated with late-onset asthma/atopy
Vasculitis - Ix
BEDSIDE
- BP & urine dip = essential (renal involvement often determines prognosis).
- Microscopy if abnormalities
BLOODS
- FBC – leucocytosis in primary disease/infection, leucopaenia in CTDs
- LFTs – hepatitis is a common secondary cause of vasculitis
- Inflammatory markers
IMMUNOLOGY:
=> c-ANCA associated with Wegener’s
=> p-ANCA associated with Churg-strauss syndrome and microscopic polyangiitis
FURTHER TESTS:
- Tissue biopsy – essential to confirm diagnosis (exclude infection) before treatment with potentially toxic immunosuppressants.
- Skin biopsy
- Renal biopsy if there are urine dip abnormalities
Vasculitis - Mx
Depends on the size of vessel involved.
- Corticosteroids are the mainstay of treatment.
=> Prolonged dose reduction over 12 months - Cyclophosphamide (low-dose or pulse) is often used in ANCA-positive disease to induce remission (but can lead to infertility)
- IVIG is often used in Kawasaki disease
- Plasma exchange may be used in life-threatening disease.
Hypermobility syndrome - presentation
= the ability to move the joints more than the normal population.
Can be asymptomatic, or can cause some people pain, fatigue, and injuries to joints and ligaments
Who gets hypermobility syndrome?
Up to 10% of the population are hypermobile, particularly women.
It is generally an inherited trait.
Certain diseases are associated with hypermobility:
=> E.g. Marfan’s, Ehlers-Danlos syndrome, Down’s syndrome
Hypermobility - diagnosis
Beighton Score – scores >6 indicate hypermobility
Approach to Assessing Fractures
- A to E Assessment
- History & Examination
• Ascertain mechanism and site
• Associated injuries
• Joint symptoms
• Neurovascular status
• Contaminated? - Radiology:
• Order two plain film orthogonal views (as well as the joints above and below the injury)
• CT/MRI if the fractures are poorly visualised on XR
Describing a Fracture on X-ray
- Skin
=> Open or closed fracture? - Bone
=> Which side?
=> Where? – mid-shaft / base / head / neck
=> Joint involvement? – intra or extra-articular - Configuration:
=> Simple or multi-fragmentary (>3 pieces)?
=> If simple, is it transverse / spiral / oblique? - Displacement:
=> Is there any?
=> Type of displacement (described in terms of distal part related to proximal part). - Mobilisation / immobilisation:
=> Is it stable or does it require immobilisation?
Terms for displacement of a fracture
• Angulation = fragments are tilted in relation to each other
• Translation = bones shifted sideways/back/forwards
• Rotation = rotation of the distal fracture fragment (often hard to see on XR)
• Shortening = bones overlap
Greenstick fractures
can occur in children due to their malleable bones.
The bone fractures on one side and buckles/is bent on the other side.
Reduction is easy and healing is quick.
Salter Harris classification
= used for fractures at the growth plate
I (S) Straight through growth plate
II (A) Above growth plate
III (L) Lower than growth plate
IV (T) Through Growth Plate
V (ER) Erasure of Growth Plate
I, II => Splinting or Casting
III, IV => ORIF
V => Surgery
RFs for fractures
Osteoporosis /osteomalacia /Paget’s
Primary / metastatic neoplasia
Bone cysts
Congenital diseases (e.g. osteogenesis imperfecta)
Mechanism of fracture repair in unstable conditions
- INFLAMMATION (1-7 days) – the fracture ends bleed, leading to haematoma formation around the fracture site and an inflammatory response creating a fibrin & capillary network.
- SOFT CALLUS (1-3 weeks) – as movement of the fracture ends is reduced, the vascular network expands, and fibrous tissue replaces the haematoma. Subperiosteal new bone formation begins.
- HARD CALLUS (1-4 months) – calcification of the soft callus takes over 1-4 months, forming rigid calcified tissue.
- REMODELLING – once the fracture is solidly united, remodelling takes place over the following months to years, with the new woven bone being replaced by lamellar bone, and medullary canal being restored.
Mechanism of fracture repair in unstable conditions
- INFLAMMATION (1-7 days) – the fracture ends bleed, leading to haematoma formation around the fracture site and an inflammatory response creating a fibrin & capillary network.
- SOFT CALLUS (1-3 weeks) – as movement of the fracture ends is reduced, the vascular network expands, and fibrous tissue replaces the haematoma. Subperiosteal new bone formation begins.
- HARD CALLUS (1-4 months) – calcification of the soft callus takes over 1-4 months, forming rigid calcified tissue.
- REMODELLING – once the fracture is solidly united, remodelling takes place over the following months to years, with the new woven bone being replaced by lamellar bone, and medullary canal being restored.
Mechanism of fracture repair in absolute stable conditions
If surgical intervention leads to ABSOLUTE STABILITY of the fracture site, the bone ends that are in contact with each other heal without callus formation.
What are the potential acute complications of fractures?
Compartment syndrome
Visceral injury – e.g pneumothorax in rib fracture, bladder injury in pelvic injury
Nerve injury
Vascular injury (suggested by the 6Ps; perform angiogram if suspected)
Infection (more likely with open fractures)
Rhabdomyolysis
=> Screened for with a CK in all patients with a crush injury or a long lie
Bleeding – large amounts of blood can be lost from long bone fractures.
What is Compartment Syndrome?
Bleeding, oedema or inflammation can cause increased pressure in an osteofascial compartment, resulting in muscle ischaemia +/- nerve necrosis
The forearm and lower leg flexor compartments are most commonly affected.
Compartment Syndrome - Presentation
“Worst ever” pain, may be described as “bursting”
Pain not relieved by strong opioid analgesia.
There is often still a pulse as the pathology is capillary/venous based and the limb is often still warm and red.
Compartment Syndrome - Ix
CLINICAL DIAGNOSIS
If the diagnosis is in doubt, compartmental pressure catheters can be used.
=> If compartment pressure is >30mmHg over DBP then immediate decompression is required.
Compartment Syndrome - Mx
Remove casts / bandages / dressings
Elevate limb
Immediate fasciotomy if high clinical suspicion or positive pressure readings.
Debridement if any necrosis present
Aggressive IV fluids (due to risk of myoglobinuria and AKI)
Leave wound open and inspect after 2 days for potential closure.
Late complications of fractures
Infection (including HAP)
DVT/PE
Pressure sores
Delayed union
Non-union
Malunion
Avascular necrosis
Joint instability
OA
Complex regional pain syndrome
Fractures - Delayed Union
= When a fracture takes longer than expected to heal for an injury of its type
RFs = same as those for poor healing
Clinical features:
- Persisting fracture tenderness
- On XR => fracture line still visible, with very little callous formation.
Tx:
=> Eliminate any possible cause, immobilise in plaster but promote muscular exercise within the cast to encourage union.
Fractures - Non-union
= when the fracture will never unite without intervention.
=> Diagnosed when not healed after 2x the usual expected time
Clinical features:
- Movement that can be elicited at the site.
- Pain diminishes as the site gap becomes a pseudoarthrosis
Fracture non-union on X-ray
On XR the fracture is clearly visible
- Hypertrophic non-union – fracture ends are enlarged
- Atrophic non-union – fracture ends tapered, with no suggestion of new bone formation.
Fracture non-union - Mx
Conservative = splinting or functional bracing
Surgical = rigid fixation +/- bone grafting
Fractures - malunion
The bones unite, but in an unsatisfactory position (rotation / angulation / shortening), due to inadequate reduction or immobilisation.
There is usually an obvious deformity, although rotation deformities can be missed.
Tx:
- Re-manipulation, osteotomy and internal fixation
- Or Limb-lengthening procedures.
Distal Radius Fracture with Dorsal Angulation
AKA Colles’ type fracture
= a fracture of the distal radius with dorsal displacement of the distal fragment
Classically caused by a FOOSH
What is the most common pattern of fracture seen in the wrist?
= Colles’ type fracture
what is considered a “distal radius” fracture?
A fracture within 4cm of the radio-carpal joint
Colles’ type fracture on XR
Dorsal displacement of the radius and radial impaction (leading to a shortened radius compared to the ulna).
=> “Dinner fork deformity”
Colles’ type fracture - Mx
Should initially be manipulated, with traction and application of a moulded plaster to maintain the reduction
If a good position has been achieved, then a trial of conservative management may be appropriate, with X-rays at week 1 and 2 to confirm position.
Unstable/comminuted fractures usually need definitive management (ORIF)
Complications of Colles’ type fracture
median nerve damage
post-traumatic carpal tunnel syndrome.
Distal Radius Fracture with Volar Angulation
AKA Smith’s type fracture
= a fracture of the distal radius with volar displacement of the distal fragment
Caused by fall onto flexed wrist
Much less common than Colles’ fractures, and usually much more unstable
Smith’s Type Fracture - Mx
Generally always require ORIF
Scaphoid Fracture - causes and presentation
Typically caused by violent hyperextension of wrist (e.g. FOOSH)
Pain is maximal in the anatomical snuff box and the pinch grip is weak.
Scaphoid Fracture - Ix
IMAGING = Scaphoid XR series should be ordered => AP, lateral and two oblique views.
notoriously difficult to pick up on X-ray !!!
Scaphoid Fracture - Mx
If the initial X-rays look normal, but clinical suspicion is still very high
=> Pt should still be treated as a fracture patient with repeat X-rays out of plaster at 2 weeks and repeat clinical examination.
UNDISPLACED FRACTURES:
- Conservative – immobilisation in thumb spica (forearm plaster including the thumb) for 6-8 weeks.
- The patient should be warned that there is up to 10% risk of non-union which may require surgical intervention.
Scaphoid Fracture - Mx
If the initial X-rays look normal, but clinical suspicion is still very high
=> Pt should still be treated as a fracture patient with repeat X-rays out of plaster at 2 weeks and repeat clinical examination.
UNDISPLACED FRACTURES:
- Conservative – immobilisation in thumb spica (forearm plaster including the thumb) for 6-8 weeks.
- The patient should be warned that there is up to 10% risk of non-union which may require surgical intervention.
Scaphoid Fracture - complications
Avascular Necrosis is a common complication due to retrograde blood supply
Forearm Fractures
Can be simple, or associated with dislocations.
Most commonly a Monteggia fracture
=> Proximal ulna fracture + radial head dislocation
Galeazzi fractures are less common
=> Fracture of radius
=> Dislocation of distal radio-ulnar joint
What are Galeazzi fractures often associated with?
radial nerve injury, or extensor tendon injuries leading to wrist drop
NOF - presentation
usually post-fall in the elderly
If the fracture is displaced, the patient lies with the limb shortened and externally rotated
Hip pain on passive movements
Blood supply to the hip joint
- Intramedullary vessels – run inside the medullary canal
- Medial/lateral circumflex artery anastomoses – from the profunda femoris, run proximally through the joint capsule up to the femoral head.
=> MOST IMPORTANT SUPPLY - Artery of ligamentum teres – makes up <10% of normal blood supply
Impact of #NOF on blood supply to the hip
All fractures of the neck of femur disrupt the intramedullary blood supply.
Any displaced fractures will also disrupt blood supply from the circumflex arteries within the capsule
The remaining supply from the ligamentum teres is insufficient.
Intracapsular NOF #
Occur proximal to the capsular insertion on the femoral neck (just above the intertrochanteric line).
Garden criteria are used to grade these fractures from 1-4, based on the degree of displacement
Garden criteria for intracapsular NOF #
Garden 1 = Incomplete; impacted fracture
Garden 2 = Complete fracture across the neck, but not displaced.
Garden 3 = Complete fracture; some continuity between the fracture ends.
Garden 4 = Complete fracture; no continuity between fracture ends.
Intracapsular NOF # - Mx
(depends on degree of displacement and fitness of patient)
Garden 1-2 – ORIF; low-risk of AVN so fixed with cannulated hip screws.
Garden 3-4 – Hemiarthroplasty** (or THR); high risk of AVN
Young Trauma Patients should have ANY fracture screwed (due to the need for multiple revisions should they have a hemiarthroplasty)
=> If AVN develops, they will tolerate the revision surgery much better than elderly patients
=> Need follow up for 2 YEARS for AVN.
** Patients that are mobilising well outside and good with ADLs should have a THR rather than hemiarthroplasty, due to their high functional demands giving this surgery better outcomes
Conservative Mx may be used if elderly, non-ambulatory, with multiple co-morbidities.
Intertrochanteric NOF #
Fracture lies between the trochanters, and are therefore extracapsular.
=> No threat to blood supply of femoral head
Intertrochanteric NOF # - Mx
Dynamic hip screw
=> fracture reduced on a traction table in theatre, then a guide-wire positioned under fluoroscopic guidance before the DHS then fixed.
Subtrochanteric NOF #
Occur below the trochanters, thus again are extracapsular and do not pose a threat to femoral head blood supply.
Generally occur in high energy trauma, or as a result of lytic lesions.
Subtrochanteric NOF #
Intramedullary nail and hip screw
Approach to hip fracture patients
- A full “falls history”
- Ask about any previous fractures / bone pain prior to fall
- Ask how long the patient was on the floor for
- Investigations:
a. Bloods – including coagulation and G&S
b. ECG & CXR
c. AP Pelvis / lateral hip X-Ray
=> Image whole femur if suspecting pathological fracture
NOF prognosis
10-20% of patients will require a change to a more dependent residential status.
Patients should mobilise within the 1st 24h for best outcomes.
Vertebral wedge fracture
- mechanism
- presentation
can occur with minimal trauma in osteoporosis.
Mechanism of injury = excessive spinal flexion, whilst posterior ligaments remain intact, leading to anterior fractures.
Presentation:
- Marked pain, worse on movement and weight-bearing
- Pain will slowly improve over months.
The fracture is very stable (as only the anterior column is affected), however multiple of such fractures can lead to a kyphotic deformity of the lumbar spine
Vertebral Wedge # - Ix
AP and lateral X-rays of the spine
Vertebral Wedge # - Mx
Bed rest for 1-2 weeks
Conservative – mobilisation and muscle strengthening exercises; (brace if >25% anterior height reduction).
Surgical – kyphoplasty (cement is percutaneously injected into the collapsed vertebrae)
What C-spine fractures are there?
Jefferson’s fracture (C1)
Hangman’s Fracture (C2)
Odontoid fractures
Tibial Fracture - Ix
XR:
=> Remember to ensure whole length of tibia and fibula are imaged, as well as the knee and ankle joints.
Tibial Fracture - Mx
MINIMALLY / UNDISPLACED
can be treated with a full-length cast
=> Mid-thigh to metatarsal necks, knee slightly flexed, ankle at 90o.
DISPLACED
will require reduction under GA with XR guidance before full-length cast application.
- The limb is elevated and observed for 48h for signs of compartment syndrome.
- The position should be checked with XR at 2 weeks.
- At 4 weeks, change to a below knee cast to allow some weight bearing (promotes healing).
Ankle # - presentation
OE – intense pain and inability to stand
Ankle fracture - Ix
AP, lateral and “mortoise” (oblique film facing inferior tibiofibular joint) X-ray views
Weber A Ankle #
Fracture below level of syndesmosis; syndesmosis remains intact.
Weber B Ankle #
Fracture at level of syndesmosis; may remain partially intact.
Weber C Ankle #
Fracture above level of syndesmosis; syndesmosis will generally not be intact.
Ankle # - Mx
Weber A fractures – generally stable and thus rarely require operative Mx; 6 weeks POP cast usually sufficient.
Weber C fractures – never stable; thus require ORIF if the patient is fit for surgery.
Weber B fractures – a trial of conservative Mx is often tried; with repeat X-rays at week 1, 2 and sometimes 3.
Fractures of >1 malleoli are almost always unstable and thus management is surgical.
Ottowa Ankle Rules
An X-ray of the ankle is required only if the patient is unable to weight bear, has pain AND bony tenderness at the lateral or medial malleolus.
An X-ray of the foot is required only if the patient is unable to weight bear AND has bony tenderness over the navicular or base of 5th metatarsal.
General Mx of long bone fractures (closed)
- ABCDE resuscitation
- Pain relief
- Image the length of the bone, as well as the joint above and below.
- Manipulation & stabilisation in POP
- Re-image to check positioning
- Check for complications – distal neurovascular status
- Further Mx depends on positioning after manipulation.
=> If the fracture has been well-reduced, conservative Mx may be used.
=> If not, surgical Mx will be indicated.
General Mx of long bone fractures (open)
- ABCDE Resuscitation
- Pain relief
- Check distal neurovascular status, and assess degree of soft tissue injury
- IV ABX started immediately +/- tetanus prophylaxis
- Imaging
- Theatre within 6 hours for definitive management and irrigation
=> Plastic surgery input may be required
What is SLE?
Who does it typically affect?
= an autoimmune condition, with autoantibodies directed at a range of tissues
Affects young and middle aged women, particularly of Asian descent.
SLE - presentation
Presentation is extremely varied, due to the number of organ systems involved
FATIGUE and PAIN are often a predominant feature alongside various other symptoms
(Skin, CNS, renal, MSK, Lung, Heart. haematological)
SLE - Skin involvement
Chronic discoid LE – red, scaly plaque, usually on the face/scalp.
Malar rash – symmetrical, raised erythematous rash across the cheeks and bridge of nose (spares nasal cleft).
Photosensitivity reactions – rashes in sun-exposed areas (in either malar or discoid patterns).
Alopecia
20% will also have oral mucosal lesions, with superficial erosions and ulcers.
SLE - CNS involvement
Non-organic disorders are most common – e.g. depression and anxiety.
Organic brain disorders – e.g. epileptic seizures.
Vascular occlusion and infarction can occur in APL syndrome.
SLE - renal involvement
Glomerular disease that can follow many patterns (most commonly interstitial nephritis).
SLE - haematological involvement
Normocytic hypochromic anaemia.
Thrombocytopaenia – due to antiplatelet antibodies
Leucopaenia
Occasionally can be autoimmune haemolytic anaemia due to red cell antibodies (positive Coomb’s test).
SLE - MSK involvement
Arthritis (90%), usually beginning in the fingers, wrists and knees (often misdiagnosed as RA).
Myalgia (50%)
SLE - lung involvement
Recurrent pleurisy and pleural effusions
Pulmonary fibrosis.
SLE - heart involvement
Most commonly pericarditis
Rarer = aortic valve lesions and cardiomyopathy.
SLE patients are also at higher risk of atherosclerosis.
SLE - Ix
BLOODS:
- FBC, U&E, ESR/CRP
- ANA
- RF
- Anti-dsDNA
- serum complement levels
- APL antibodies (? comorbid APL syndrome)
Urine dip & BP to check for renal involvement
HISTOLOGY:
Characteristic histology/immunofluorescence seen in skin/kidney biopsies.
SLE - typical blood results
FBC – normocytic hypochromic anaemia, thrombocytopaenia, leukopaenia.
ESR/CRP – ESR raised; CRP often normal.
U&Es may be deranged if renal involvement
Serum ANA – almost always positive
Serum RF – positive in 25%
Anti-dsDNA – specific for SLE, but sensitivity of 50% (fluctuates with disease activity).
RNA antibodies (anti-Ro/anti-La) often present
Serum complement levels – C3/4 levels reduced in active disease
APL antibodies – positive if comorbid APL syndrome.
SLE - Mx
Patient education
Avoid sunlight / high SPF sunscreen
Modify CV risk factors
MILD DISEASE
- NSAIDs and Hydroxychloroquine.
=> Combination therapy helps skin disease, arthralgia and fatigue.
MORE SEVERE DISEASE (e.g. cardiac/renal involvement):
- Prednisolone, with DMARDs such as azathioprine for steroid sparing.
Regular Monitoring for signs of active disease:
=> History & examination
=> FBC, U&E, C3/4, urine dip
Antiphospholipid Syndrome
= the presence of autoantibodies that have a specificity for phospholipids, leading to a thrombotic tendency.
It can be a primary syndrome, or occur secondary to SLE.
APL Syndrome - Features
Venous thrombosis – most commonly in the arms/legs, leading to a risk of PE
Arterial thrombosis
=> Less common than venous thrombosis
Miscarriages
Splinter haemorrhages
Livedo reticularis (classical “lace-like” rash)
May also have – thrombocytopaenia, migraines, epilepsy
APL Syndrome - Ix
History & Examination
=> Including obstetric history (miscarriages).
ESR – usually normal
ANA – usually negative
APTT – increased
Coomb’s test – positive
Anticardiolipin antibodies = diagnostic
=> Need high titres required on 2 occasions, 12 weeks apart.
Lupus anticoagulant antibodies – present in 20%
=> Represent an increased risk of thrombosis
What test is diagnostic for APL Syndrome?
Anticardiolipin antibodies
APL Syndrome - Mx
Those with a history of severe thrombosis:
=> Warfarin – target INR 3-4 to stop arterial thrombosis.
Those without a thrombotic history:
=> Low-dose aspirin
=> Lifestyle advice to avoid prolonged immobilisation and oestrogen-containing drugs.
LMWH and aspirin are given in pregnancy, and an early delivery is often planned for under specialist care.
Prognosis of APL Syndrome
Long-term prognosis is poor, with 1/3rd having organ damage within 10 years of diagnosis.
What are the idiopathic inflammatory myopathies?
- Polymyositis
- Dermatomyositis
- Inclusion body myositis
What can polymyositis and dermatomyositis be associated with?
HLA-B8/DR3 genotype
SLE, RA or systemic sclerosis
Both are associated with various malignancies.
What is polymyositis?
How can it present?
= Inflammation of striated muscle, causing proximal muscle weakness.
- Generally causes weakness in the absence of pain
- There may be associated muscle wasting
- Onset can be insidious or acute
- It is associated with malaise, weight loss and fever
- The patient will have difficulty squatting or climbing stairs.
If left untreated, respiratory muscle involvement can lead to respiratory failure.
What is dermatomyositis?
Polymyositis with associated skin involvement.
Classic heliotropic rash (i.e. purple discolouration around the eyelids).
Associated periorbital oedema.
Vasculitic patches over the knuckles (Gottron’s papules).
Dermatomyositis/Polymyositis - Ix
Bloods:
- Serum CK – raised, reflecting muscle damage.
- ESR – rarely raised
- ANA – most are positive
- RF – 50% are RF positive
- Myositis specific antibodies
Electromyography:
- EMG shows a characteristic pattern
MRI:
- To detect areas of abnormal muscle.
Needle Muscle Biopsy:
- Shows fibre necrosis with inflammatory infiltrate.
Further investigations as appropriate to screen for malignancy.
Dermatomyositis/Polymyositis - Mx
Prednisolone / DMARDs until myositis is clinically inactive.
IVIG therapy may be used in some cases.
Inclusion Body Myositis - Sx, Ix, Mx
Typically affects white males over 50
Insidious onset of proximal and distal muscle wasting, which may be symmetrical.
Ix:
- ANA is less frequently positive
- Myositis-specific antigens will not be positive.
- Muscle biopsy shows inflammatory infiltrate and vacuoles containing beta-amyloid (“inclusion bodies”)
It is progressive, and rarely responds to prednisolone/DMARD combinations.
Indications for synovial fluid analysis
?acute bacterial septic arthritis
=> send for MC&S
?crystal associated disease
=> send for polarised light microscopy
Clear/straw-coloured joint aspirate
= normal synovial fluid
Turbid joint aspirate
indicates inflammation (due to an increase in cell count (particularly neutrophils)
will be less viscous than normal (degranulation of inflammatory cells digests the normal proteins)
Turbid fluid should be analysed with an urgent gram stain, and then culture.
=> Culture takes 48h, so treat sepsis first.
Uniformly blood-stained joint aspirate
may be due to trauma, severe inflammation of any kind, or bleeding tendencies.
Non-uniform blood-stained joint aspirate
indicates a traumatic aspiration.
Polarised light microscopy for ?crystal arthropathy
MSU Crystals – needle shaped, negatively birefringent = GOUT
CPPD Crystals – rhomboid shaped, positively birefringent = PSEUDOGOUT.
What rheum conditions can cause thrombocytopaenia?
Due to:
- disease activity in SLE/APL
- Felty’s Syndrome in RA
- drugs such as methotrexate.
How can rheum conditions cause anaemia?
Due to:
- chronic disease,
- iron deficiency,
- megaloblastic anaemia (due to methotrexate)
- haemolysis (SLE/drugs).
What is rheumatoid factor?
= IgM antibody against IgG, forming immune complexes that contribute to the disease process.
What does positive rheumatoid factor indicate?
Positive in 70% of people with RA
=> 78% specific – also raised in SLE/Sjogren’s
=> Can be transiently raised in infections or just in normal population
Indicates a worse prognosis (and extra-articular manifestations) if positive at diagnosis.
Anti-CCP
= 90-98% specific for RA; 60% sensitive
It may precede the onset of RA by 12 years.
Indicates a worse prognosis if raised at presentation.
Anti-Nuclear Antibody (ANA)
Titres >1:80 are considered positive but are generally >1:320 in autoimmune disease.
Useful to r/o SLE, which has nearly 100% ANA positivity.
Also can be raised in RA, Sjogren’s, Scleroderma, polymyositis.
Anti-dsDNA
Specific for SLE, but often only present in severe disease.
Marker for poor prognosis (indicates renal involvement).
Level changes with disease activity, so can be used as a marker
Extractable Nuclear Antigens (ENA) Panel
Anti-Sm is specific to SLE
Anti-Ro & Anti-La are often present in Sjogren’s (but also SLE)
Some ENAs can be used to indicate specific tissues involved:
- E.g. Anti-Jo1 in myositis indicates pulmonary fibrosis.
- E.g. Antitopoisomerase in scleroderma indicates pulmonary/cardiac involvement.
Generally there is no use for longitudinal ENA monitoring
What is systemic sclerosis?
What are the subtypes?
= A multi-system autoimmune disease, characterised by skin sclerosis and Raynaud’s disease.
- Limited Cutaneous Systemic Scleroderma (~70% cases)
- Diffuse Cutaneous Systemic scleroderma (~30% cases)
Limited cutaneous systemic sclerosis - Sx
Patients present with a long history of Raynaud’s phenomenon, then skin tightening at the extremities
=> Typically the fingers and toes are affected; Can also occur on the face, leading to microstomia.
EARLY:
Fatigue
GORD
Ulcers on digital tips
LATE:
Oesophageal strictures
Small bowel malabsorption
Pulmonary fibrosis / pulmonary HTN
What was limited cutaneous systemic sclerosis previously know as?
Why was this abandoned?
Previously known as CREST Syndrome
- C – Calcinosis
- R – Raynaud’s
- E – Oesophageal dysmotility
- S – Sclerodactyly
- T – Telangiectasia
This term was abandoned as it under-emphasises life threatening complications such as pulmonary HTN.
Limited cutaneous systemic sclerosis - Mx
Digital sympathectomy / vasodilators
Removal of calcinoses
Tx of oesophageal problems
Diffuse cutaneous Systemic Sclerosis - Sx
Patients have a short Hx of Raynaud’s disease, and skin sclerosis is rapidly progressive.
Systemic symptoms are greater, including lethargy, weight loss and anorexia.
Complications will occur within the first 3 years:
- Myocardial fibrosis
- Pulmonary fibrosis
- Renal fibrosis
Diffuse Cutaneous Systemic Sclerosis - Mx
Immunosuppression – aiming to prevent complications, so can be gradually withdrawn over years as the disease stabilises.
Again, sympathectomy and vasodilators are helpful for symptoms.
Systemic Sclerosis - Ix
Limited cutaneous systemic scleroderma:
=> Anti-centromere antibodies positive (60%)
Diffuse cutaneous systemic scleroderma:
=> Anti-Scl-70 antibodies (40%) and RNA polymerase antibodies
Systemic Sclerosis - prognosis
Systemic sclerosis has the highest mortality of any of the autoimmune rheumatic diseases.
Limited cutaneous scleroderma has a higher survival (70% at 10 years), due to less severe internal organ damage.
Overuse/strain injury - presentation
• Exact time/mechanism of injury can be identified.
• Pain is non-progressive and produced by one/few movements.
• O/E:
=> localised tenderness
=> pain reproduced on resisted active movement/stress testing.
What is De Quervain’s Tenosynovitis?
= Painful inflammation of the abductor pollicis longus and extensor pollicis brevis tendons in the 1st dorsal compartment of the wrist.
The 1st dorsal compartment is just proximal to the anatomical snuff box.
unknown cause
De Quervain’s - Presentation
- Often acute pain over the 1st dorsal compartment when using the thumb
- Swelling/tenderness over the area.
- Most common after unaccustomed intensive activity (e.g. painting a fence)
- Classically affects middle-aged, post-partum women.
De Quervain’s - O/E
LOOK – often normal, may have swelling over radial border.
FEEL – may be normal; or tender over radial border.
MOVE – active thumb abduction/opposition and active ulnar deviation may be affected.
TEST – Finklestein’s test positive.
De Quervain’s - Mx
Conservative:
• Most presentations respond well to rest, analgesia and splints
• Thumb immobilisation with splints for 3 weeks
• Steroid injections can also be used.
Surgical:
• Rarely used; longitudinal compartment release.
Median Nerve Compression / Carpal Tunnel Syndrome
= a compression neuropathy of the median nerve as it passes though the carpal tunnel.
(It is technically median nerve compression until there is thenar eminence wasting, at which point it can be called carpal tunnel syndrome.)
Anatomy of the Carpal Tunnel
The carpal tunnel consists of the carpal bones, covered by the floor of the flexor retinaculum.
It contains 9 flexor tendons (4 FDP, 4 FDS, and 1 FPL) and the median nerve
Carpal Tunnel Syndrome - causes
Most cases are idiopathic
Entrapment often seen in a range of conditions – DM, RA, hypothyroidism, acromegaly, trauma (Colles’ fracture).
Carpal Tunnel Syndrome - presentation
Pain/paraesthesia in the hand, worst in the morning (due to wrist flexion when asleep).
May wake the patient from sleep, and they shake the hand/hang it over the side of the bed for relief.
Thenar muscle weakness/wasting
=> First noticed as clumsiness, due to loss of opposition strength.
Sensory loss in palm / radial 3 ½ fingers (rarely noticed).
Carpal Tunnel Syndrome - O/E
LOOK – thenar wasting in advanced cases, otherwise nil.
FEEL – potentially reduced thenar bulk
MOVE – active thumb abduction and active thumb opposition affected.
TEST
• Positive Tinel’s
• Positive Phalen’s
• Test sensation between sides and between dermatomes on same side.
Carpal Tunnel Syndrome - Ix
Typically diagnosed from Hx and Examination
Nerve conduction studies can show slowing at the wrist, but can also be normal.
Carpal Tunnel Syndrome - Mx
Conservative – rest, night time splinting, NSAIDs / steroid injections to reduce inflammation around the tunnel.
Surgical – division of flexor retinaculum (carpal tunnel release)
=> leads to scar on wrist.
Cubital Tunnel Syndrome
Compression neuropathy of the ulnar nerve at the cubital tunnel of the elbow.
This can be compressed if the patient has flexed elbows for long periods or due to tight fascial bands, ulnar fracture, valgus deformities of the elbow or other pathology.
Cubital Tunnel Syndrome - Presentation
Pain near elbow joint, may radiate down ulnar border of forearm
Paraesthesia and sensory loss over ulnar distribution.
Hand clumsiness and reduce pinch / grip strength
If severe, clawing of the hand due to wasting of hypothenar and interosseus muscles.
Cubital Tunnel Syndrome - O/E
LOOK – guttering between metacarpals, hypothenar wasting.
FEEL – tenderness around cubital tunnel
MOVE – elbow movements may be limited; the Pt may be unable to actively extend at the IPJs or actively abduct/adduct the finger
TEST
• Loss of sensation
• Reduced first dorsal interosseus power
• Positive Tinel’s test along length of ulnar nerve
• Positive elbow flexion test (sustained elbow flexion, with arm supinated and wrist extended reproduces symptoms)
Cubital Tunnel Syndrome - Ix
X-rays may show pathogenic osteophytes
Nerve conduction studies may show slowing at the elbow.
Cubital Tunnel Syndrome - Mx
Conservative – night time splints, NSAIDs, activity modification.
Surgical – simple cubital tunnel decompression, or anterior transposition of the nerve.
What is a ganglion cyst?
Soft tissue swellings filled with a degenerative myxoid fluid that stems from an underlying joint capsule or ligament of tendon sheath.
Can be idiopathic or caused by trauma.
Ganglion Cyst - Presentation
Lump in hand/wrist => cosmetic concerns
Sometimes pain
Ganglion Cyst - O/E
LOOK – most common sites are dorsum of wrist (scapholunate joint), volar aspect of wrist (scaphotrapezial joint), at the base of finger from the flexor sheath or at the DIPJ.
FEEL – may be hard or soft, but are never fixed to the skin
MOVE – may become more obvious with joint movements or limit end range.
TEST – will transilluminate.
Ganglion Cyst - Mx
Conservative – NSAIDs and reassurance; aspiration +/- steroid injections have a 40% success rate.
Surgical – excision leads to a 40% recurrence rate.
What is trigger finger?
Idiopathic fibrosis of the flexor tunnel, leading to an intra-tendinous nodule that interrupts normal finger movement.
Usually involves ring/middle finger
The Pt complains that the finger gets stuck in flexion, then on further effort (can involve using the other hand) can snap into extension.
In severe cases the finger can be permanently locked.
RFs for trigger finger
Occurs most commonly in women >40.
RA
DM
Trigger Finger - O/E
LOOK – potential flexion at the PIPJ/DIPJ
FEEL – can feel the triggering of the flexor tendons by placing your finger in the palm and asking the patient to flex the finger; a nodule is often felt at the base of the finger
MOVE – jerky, hesitant active flexion/extension
Trigger Finger - Mx
Conservative – usually resolves spontaneously with:
- Activity modification,
- NSAIDs,
- Tendon sheath corticosteroid injection.
Surgical:
- Release of the A1 pulley
- Tenosynovectomy in RA
What is Dupytren’s Contracture?
Progressive, painless thickening of the palmar fascia
causes flexion deformities of fingers and functional difficulties.
Dupytren’s Contracture - RFs
More common in males, Nordics & those with FHx
May be linked to trauma, diabetes, alcoholism, phenytoin, liver cirrhosis
Dupytren’s Contracture - O/E
LOOK – nodules/cords in the palm and fingers, flexion of MCP and PIP joints, classically affecting the middle and ring fingers
FEEL – thickened palmar fascia, “Garrod’s” pads on the dorsum of PIPJs
MOVE – loss of active and passive extension of involved joints
TEST – n/a
Dupytren’s Contracture - Mx
No specific Tx required if the patient has no functional impairment
Surgical – needle aponeurotomy, enzymatic fasciotomy, fasciotomy, fasciectomy, dermo-fasciectomy.
Base of thumb OA - presentation
Patients present with pain on activities involving gripping/pinching, with swelling, deformity and tenderness at the CMCJ.
Base of thumb OA - O/E
LOOK – “squaring” of thumb, base of thumb swelling, wasting of thenar muscles.
FEEL – may be pain/warmth in the joint, reduced thenar bulk
MOVE – global pain/stiffness of CMCJ movements (adduction, palmar/radial adduction, opposition).
Base of thumb OA - Mx
Conservative – as for any OA patient
Surgical – denervation, trapeziectomy, basal thumb arthroplasty or joint fusion.
Medial Epicondylitis
GLOFER’S ELBOW
Tendinopathy of the common flexor-pronator origin, just distal to the bony prominence of the medial epicondyle.
Caused by recurrent microtrauma (such as golf swings placing stress on the elbow joint).
Medial Epicondylitis - Presentation
Pain develops subacutely over a period of weeks to months, exacerbated by use and settled with rest.
The pain can be very severe, and can radiate up/down the arm (especially when using the affected muscles, e.g. carrying a tray).
Medial Epicondylitis - O/E
Tenderness around the medial epicondyle
Pain triggered by resisted flexion of the hand.
Normal ROM, no neurological Sx (such as tingling/numbness, if so, consider ulnar nerve entrapment).
Medial Epicondylitis - Mx
CONSERVATIVE:
- Simple Analgesia (NSAIDs) and rest
- Referral to physiotherapy (strengthening exercises)
- Epicondylar clasp (provided by splint department).
- Steroid injection
If all of the above unsuccessful => X-ray of joint to r/o OA.
If conservative measures fail, golfer’s elbow release can be performed surgically.
Lateral Epicondylitis
TENNIS ELBOW
Tendinopathy of the common extensor tendon origin, just distal to the lateral epicondyle.
Can be caused by repetitive gripping/grasping movements.
Much more common than Golfer’s Elbow
RFs for Lateral Epicondylitis
- Peak incidence ~40-60 years.
- Obesity,
- Smoking
- Carpal tunnel syndrome and other tendinopathies.
Lateral Epicondylitis - Presentation
Pain around the lateral epicondyle, develops subacutely.
Typically exacerbated by movement and relieved by rest.
Pain may radiate up/down the arm, worse by holding heavy bags etc.
Lateral Epicondylitis - O/E
Point tenderness distal to the lateral epicondyle
Pain can be reproduced on resisted extension of wrist.
Passive ROM is normal
Lateral Epicondylitis - Mx
Conservative = as for medial epicondylitis.
Surgical intervention = tennis elbow release (if conservative measures fail).
Lateral Epicondylitis - Mx
Conservative = as for medial epicondylitis.
Surgical intervention = tennis elbow release (if conservative measures fail).
Olecranon Bursitis
Olecranon bursa becomes enlarged as a result of pressure or friction.
It is NOT a painful condition
=> If pain is present, consider differentials such as gout/RA/infection
What are some common differentials for shoulder pain?
• Acute (calcific) rotator cuff tendonitis
• Chronic rotator cuff tendonitis
• Rotator cuff tear
• Adhesive capsulitis
• Subacromial bursitis
• Cuff arthropathy
• Osteoarthritis
• RA
• Polymyalgia rheumatica
What is Acute Rotator Cuff Tendonitis (Calcific Tendonitis)?
= Deposition of apatite (basic calcium phosphate) in the supraspinatus tendon, leading to an intense inflammatory reaction and swelling.
Acute Rotator Cuff Tendonitis - Presentation
- Young patients, complaining of aching pain following over-use.
- Pain increases to an intense climax, before resolving in a few days.
- The arm is held immobile and the joint is often too tender to palpate.
- XR will show calcification just above the greater tuberosity.
Acute Rotator Cuff Tendonitis - Mx
- Resting the arm in a sling
- NSAIDs
- More severe pain may require intra-capsular corticosteroid/lignocaine injection.
Usually resolves after 1-3 weeks.
What is Chronic Rotator Cuff Tendonitis?
Over-use or minor tears of the rotator cuff initiate a subacute/chronic vascular response leading to pain and stiffness
Chronic Rotator Cuff Tendonitis - Presentation
Pain in the shoulder, characteristically worse at night and when abducting/elevating the arm.
Tenderness beneath the anterior edge of the acromion
Painful arc present (60-120 degrees), with less pain when passively abducted.
Power is normal despite pain (separates it from a tear).
Chronic Rotator Cuff Tendonitis - Ix
XR may show calcification from former events, but MRI/USS are diagnostic.
Chronic Rotator Cuff Tendonitis - Mx
NSAIDs
Corticosteroids and physiotherapy if severe
If conservative measures fail, arthroscopic “decompression” of the rotator cuff can take place.
=> Excision of the coraco-acromial ligament and any osteophytes.
Rotator Cuff Tear
Caused by trauma in the younger patient (e.g. falling on arm) or can happen spontaneously in the elderly (e.g. lifting something up).
PARTIAL tears frequently occur with (and may precipitate) chronic tendonitis, but can repair naturally.
COMPLETE tears will not naturally repair.
Rotator Cuff Tear - Presentation
Patient will describe a “sprain” of the shoulder, with limited abduction after the event.
Rotator Cuff Tear - O/E
Tenderness over the anterior acromion.
Once the arm has been lifted over the shoulder, it can be held there by the deltoid (the abduction paradox), but when they lower the arm it suddenly drops.
Rotator Cuff Tear - Ix
Diagnosis confirmed with USS, MRI or arthroscopy.
Intra-articular anaesthetic injections can distinguish between full and partial tears:
=> Partial tears will regain abduction when the pain is abolished.
=> Similarly, partial tears will regain the ability to abduct within a few weeks, whereas full tears will not.
Rotator Cuff Tear - Mx
Acute phase – heat, exercises and local anaesthetic injections.
After 3 weeks, the extent of the rupture can be assessed.
Complete tears in younger individuals are usually surgically repaired.
Partial tears are conservatively treated to allow natural healing.
Adhesive Capsulitis - presentation
= “frozen shoulder”
- Initial progressive “deep” pain that stops the patient sleeping on the affected side, but starts to subside after a few months.
- Increasing stiffness, worsening as the pain subsides, and may last for 6-12 months.
Adhesive Capsulitis - O/E
- There are limited signs OE, as the joint cannot be moved due to pain.
- Limited external rotation is classic.
Adhesive Capsulitis - Mx
- Reassurance
- NSAIDs
- PT referral (start ASAP, usually 6 weeks)
Intra-articular steroid injections if no progress with conservative Tx
The process tends to resolve spontaneously after about 18 months.
Causes of subacromial bursitis
Often due to repetitive overhead lifting, pulling or trauma.
Subacromial Bursitis - Presentation
- Classically causes a “burning” pain (rather than a dull ache of rotator cuff pathology)
- Worse pain when lifting above the head
- Stiffness when passively abducting the arm
Subacromial Bursitis - Ix
USS/MRI to differentiate from rotator cuff pathology.
Subacromial Bursitis - Mx
Conservative – NSAIDs and avoiding exacerbating movements.
“Rotator Cuff Syndrome”
Umbrella term for pathologies such as subacromial bursitis, adhesive capsulitis, rotator cuff tear, acute/chronic rotator tendonitis
this term is used until the exact diagnosis has been confirmed radiologically.
Complications of rotator cuff pathology
- Subluxation of humeral head – loss of the cuff’s stabilising effects
- Cuff arthropathy – rotator cuff pathology leads to a less stable humeral head in the GHJ and secondary arthritis.
Painful Arc/Impingement Syndrome
rotator cuff syndrome pathologies lead to swelling and oedema, and decrease the space between the humeral head and acromion.
This leads to a painful arc (from 60-120 degrees) = IMPINGEMENT
Shoulder Impingement - articular vs peri-articular
ARTICULAR => painful on both active and passive movements.
PERI-ARTICULAR => pathology is less painful on passive movements.
What painful arc is typical for ACJ OA?
classically causes a painful high arc - 170-180 degrees
(alongside crepitus and global pain/stiffness)
=> Scarf test can be used to confirm diagnosis
What is Trochanteric Bursitis?
Inflammation of the bursa between the greater trochanter and the fascia lata, caused by acute/repetitive trauma
More common in women and active patients, bilateral in 50%
Complicates many THRs
Trochanteric Bursitis - Presentation
“Hip” pain, that may radiate down the lateral aspect of the thigh to the knee.
Pain worse on movement and at night, especially when lying on affected side.
Trochanteric Bursitis - O/E
Point tenderness when palpating the greater trochanter.
Active abduction of a slightly flexed hip will exacerbate the pain (as it tightens the fascia lata over the bursa).
Trochanteric Bursitis - Mx
1st line = Corticosteroid injections
=> If the patient is presenting post-THR, the injection should be performed in a laminar flow theatre.
Physiotherapy referral after presentation and 1st injection.
=> Exercises to stretch the fascia lata, thus relieving excessive pressure on the bursa (e.g. cross body adduction).
The above will resolve symptoms in over 2/3rd of patients.
Refractory trochanteric bursitis can be treated with surgical release of the fascia lata and excision of the bursa.
Osgood-Schlatter’s Disease
Common in adolescents
= A traction injury of the patellar ligament, leading to a prominent and tender tibial tuberosity.
Mx:
- Spontaneous recovery takes time
- Restriction of sporting activities is advised.
- Paracetamol +/- NSAIDs
- Ice packs on tibial tuberosity up to TDS (after exercise)
Meniscal Tears - causes
Classically occur when there is a twisting strain on a flexed, weight-bearing knee (hence common in footballers)
Relatively little force is required in older adults (due to fibrosis)
Degenerative tears are seen in knee OA.
What is a problem associated with meniscal tears?
The meniscus is mainly avascular (apart from the outer 1/3rd) so will not repair spontaneously after a tear, or heal after a surgical repair.
Can be associated with ACL tears
If not repaired, small avascular tears may propagate to cause secondary arthritis
Meniscal Tear - Presentation
Symptoms are initial pain, which can be intermittent and variable amounts of swelling hours later.
Swelling subsides with rest, but may recur after further trivial injury.
The loose tag of meniscus can act as a mechanical irritant if it finds its way into the intercondylar notch, causing symptoms:
=> Locking of the knee
=> Spontaneous “giving way” of the knee
Meniscal Tear - O/E
Acutely, often effusion and fixed flexion deformity, with medial joint line tenderness.
Meniscal Tear - Ix
X-ray (AP, lateral and skyline views are essential) – will be normal but to r/o fractures/OA
MRI = mainstay of imaging, picks up >90% of tears.
Meniscal Tear - Mx
Arthroscopic repair is indicated in many patients (especially if young/active)
Tears in the vascular zone are amenable to repair
If in the avascular zone (more common), then a partial meniscectomy is the Tx of choice, to prevent ongoing mechanical symptoms
Total meniscectomy is avoided due to high risk of secondary OA
Causes of Knee Ligament Injuries
occur when a force greater than the tensile strength of the ligament occurs (e.g. sporting injuries/trauma).
most common injury = ACL Tear
(MCL = 2nd most common)
it is possible for multiple ligaments to be involved
The collateral ligaments are tight in extension and loose in flexion, thus injury is most common when the knee is extended.
Knee Ligament Injuries - important history points
It is key to elicit the full mechanism (position of the knee and direction of any force applied).
Swelling in the first hour indicates complete rupture
Patients may describe a “pop” at the time of injury
Knee Ligament Injuries - O/E
There will not be a “firm” end point when testing the ligament, rather a “soft” end point as the surrounding soft tissues stop the force.
Partial tears do not give increased mobility, but instead there is pain on testing.
Lachman’s test is significantly more sensitive than anterior drawer test for ACL pathology.
Knee Ligament Injuries - Ix
X-ray (lateral, AP, skyline) – to show any displacements, exclude OA, show any fractures.
MRI – will pick up 90% of ligament injuries
Diagnostic arthroscopy – occasionally used if MRI shows intact ACL, however clinically the patient has ACL dysfunction.
Knee Ligament Injuries - Conservative Mx
Sprains/partial tears will spontaneously heal with physiotherapy, as the intact fibres splint the torn ones.
Adhesions will complicated this process if the joint is rested, so ACTIVE MOVEMENT with a brace is encouraged.
Conservative Mx is almost always the option of choice in collateral ligament pathology, unless part of multi-level injuries.
Knee Ligament Injuries - Surgical Mx
ACL – arthroscopic tendon graft repair, with the hamstring or semitendinosus used as the donor tendon.
Collateral ligaments – if being fixed surgically, should be performed within 2 weeks of the injury.
Different forms of bursitis in the Knee
- Pre-patellar Bursitis
- Infra-patellar bursitis
1&2 present with anterior knee pain and a fluctuant swelling
- Anserine bursitis
=> Can be seen in a similar position to infra-patellar bursa, but more medial (insertion of the MCL into the upper tibia)
Mx of pre-patellar or infra-patellar bursitis
Both caused by unaccustomed kneeling
Mx:
- avoidance of kneeling
- Corticosteroid injection for troublesome symptoms
Mx of anserine bursitis
- Physiotherapy
- Local corticosteroid injection.
Popliteal / Baker’s Cyst
Bulging of the posterior capsule of the knee, with synovial herniation leading to a swelling in the popliteal fossa.
It is most often caused by RA or OA
Occasionally can rupture into the muscle planes causing swelling and pain in the calf similar to DVT.
Tx if non-ruptured = aspiration, and hydrocortisone injection.
Semimembranosus bursitis
The bursa between the semimembranosus and the medial head of the gastrocnemius becomes enlarged, presenting as a painless lump behind the knee
What is Plantar Fasciitis?
What are the symptoms?
= Enthesitis at the insertion of the plantar fascia tendon into the calcaneum
Sx:
- Localised pain on walking/standing
- Midline tenderness
- pain is worse when weight-bearing in the morning
Can occur alone, or in seronegative spondyloarthropathies.
Plantar Fasciitis - Mx
Heel pads and reduced walking
Splinting of the foot in a dorsiflexed position to stretch the plantar fascia.
Most recover spontaneously over 1 year.
What is Subcalcaneal Bursitis?
What are the symptoms?
= A pressure-induced bursa under the heel, often due to tight shoes.
Symptoms:
- Similar to plantar fasciitis
- Pain is worse when weight-bearing in the morning
- However, O/E – compression of the heel pad from the sides is painful.
Subcalcaneal Bursitis - Mx
Heel pads
Reduced walking
Achilles Tendonitis
= Enthesitis at the insertion of the Achilles tendon into the calcaneus.
Can be caused by trauma, or complicated seronegative spondyloarthropathies
Sx = Pain behind the heel and leg
Mx =
- Raising shoe heel to reduce the pain
- Low pressure corticosteroid injection near the enthesis.
Tibialis Posterior Tendon Rupture
Leads to sudden pain and valgus deformity, with tenderness around the medial malleolus.
Vertebral spinous processes
each vertebra has a single spinous process, centred posteriorly at the point of the arch.
=> In cervical spine, the spinous processes are bifid.
=> In thoracic spine, these is oriented obliquely inferiorly and posteriorly.
=> In lumbar spine, these do not extend inferiorly below the level of the vertebral body.
Vertebral Transverse processes
each vertebra has two transverse processes, which extend laterally and posteriorly from the vertebral body.
In the thoracic vertebrae, the transverse processes articulate with the ribs.
anterior and posterior longitudinal ligaments
run the full length of the vertebral column to strengthen the joints of the vertebral bodies
Superficial muscles of the back
Trapezius,
Latissimus dorsi,
Levator scapulae
Rhomboids (major and minor)
Intermediate muscles of the back
Serratus Posterior Superior
Serratus Posterior Inferior
Deep muscles of the back
Splenius Capitis
Splenius Cervicis
Erector Spinae Muscles
Transversospinales Muscles
the Erector Spinae Muscles
Consists of Iliocostalis, Longissimus and Spinalis muscles (in order of most lateral to most medial).
These muscles act unilaterally to laterally flex the vertebral column and bilaterally to extend the vertebral column and head.
Anatomy of Spinal Cord
- arises cranially as a continuation of the medulla oblongata.
- travels inferiorly within the vertebral canal, surrounded by the spinal meninges containing cerebrospinal fluid.
- At the L2 vertebral level the spinal cord tapers off, forming the conus medullaris.
- The spinal nerves that arise from the end of the spinal cord are bundled together (= the cauda equina).
Where are the points of enlargement of the spinal cord?
- The Cervical enlargement:
- It represents the origin of the brachial plexus. - The Lumbar enlargement:
- Representing the origin of the lumbar and sacral plexi.
Spinal cord - layers of meninges (external to internal)
- Epidural space
- Dura Mater
- Arachnoid Mater
- Subarachnoid Space
- Pia Mater
What are the nerve roots of the cauda equina?
L2-S5
Nerve roots of Lumbar Plexus
Mainly L1, L2, L3 and L4.
It also receives contributions from T12.
What are the 6 major peripheral nerves of the lumbar plexus?
- Iliohypogastric (L1, with contributions from T12)
- Ilioinguinal (L1)
- Genitofemoral (L1, L2)
- Lateral Cutaneous Nerve of thigh (L2, L3)
- Femoral (L2, L3, L4)
- Obturator (L2, L3, L4)
Nerve roots of Sacral Plexus
S1, S2, S3 and S4.
It also receives contributions from L4 and L5.
What are the 5 major peripheral nerves of the sacral plexus?
- Superior Gluteal (L4, L5, S1)
- Inferior Gluteal (L5, S1, S2)
- Sciatic (L4, L5, S1, S2, S3)
- Posterior Femoral (S1, S2, S3)
- Pudendal (S2, S3, S4)
What are the nerve roots of the femoral nerve?
L2-L4
Motor/sensory functions of femoral nerve
MOTOR
Hip flexors
Knee extensors (quadriceps femoris)
SENSORY
cutaneous branches to the anteromedial thigh (anterior cutaneous branches of the femoral nerve) and the medial side of the leg and foot (saphenous nerve)
What are the nerve roots of the sciatic nerve?
L4-S3
Motor/sensory functions of sciatic nerve
MOTOR
Muscles of posterior thigh
Indirectly innervates (via its terminal branches) all the muscles of the leg and foot.
SENSORY
No direct sensory functions.
Indirectly innervates (via its terminal branches) the skin of the lateral leg, heel, and both the dorsal and plantar surfaces of the foot
Course of sciatic nerve
Arises from lumbosacral plexus.
Enters the gluteal region via greater sciatic foramen.
It emerges inferiorly to the piriformis muscle and descends in an inferolateral direction.
Enters the posterior thigh by passing deep to the long head of the biceps femoris.
When the sciatic nerve reaches the apex of the popliteal fossa, it terminates by bifurcating into the tibial and common fibular nerves.
Motor/sensory functions of Tibial Nerve
MOTOR
posterior compartment of the leg
the majority of the intrinsic foot muscles.
SENSORY
the skin of the posterolateral leg, lateral foot and the sole of the foot.
Tarsal Bones
= a set of seven irregularly shaped bones, in 3 rows:
- Proximal = Talus, calcaneus
- Intermediate = Navicular
- Distal = cuboid and the three cuneiforms
Talus
It transmits the weight of the entire body to the foot.
Articulates superiorly with the tibia & fibula (= ankle joint).
Articulates inferiorly with the calcaneus (= subtalar joint)
Articulates anteriorly with the navicular (= talonavicular joint)
Calcaneus
Articulates superiorly with the talus – subtalar (talocalcaneal) joint
Articulates anteriorly with the cuboid – calcaneocuboid joint
It protrudes posteriorly and takes the weight of the body as the heel hits the ground when walking.
The posterior aspect of the calcaneus is marked by calcaneal tuberosity, to which the Achilles tendon attaches.
Navicular bone
Articulates with the talus posteriorly, all three cuneiform bones anteriorly, and the cuboid bone laterally.
On the plantar surface of the navicular, there is a tuberosity for the attachment of part of the tibialis posterior tendon.
Cuboid bone
Cuboidal in shape
Lies anterior to the calcaneus and behind the fourth and fifth metatarsals.
Cuneiform bones
= Three wedge shaped bones.
They articulate with the navicular posteriorly, and the metatarsals anteriorly.
The shape of the bones helps form a transverse arch across the foot.
They are also the attachment point for several muscles
Metatarsals
They are numbered I-V (medial to lateral).
They have three or four articulations:
- Proximally – tarsometatarsal joints – between the metatarsal bases and the tarsal bones.
- Laterally – intermetatarsal joint(s) – between the metatarsal and the adjacent metatarsals.
- Distally – metatarsophalangeal joint – between the metatarsal head and the proximal phalanx.
Planages of foot
The phalanges are the bones of the toes.
The second to fifth toes all have proximal, middle, and distal phalanges.
The great toe has only 2; proximal and distal phalanges.
Intrinsic muscles in the sole of foot
10 intrinsic muscles located in the sole of the foot
=> act collectively to stabilise the arches of the foot, and individually to control movement of the digits.
All the muscles are by branches of the tibial nerve.
Ankle / talocrural joint
a hinge-type joint, permitting dorsiflexion and plantarflexion of the foot.
Formed by three bones: the tibia and fibula of the leg, and the talus of the foot
=> The body of the talus fits snugly into the mortise formed by the bones of the leg.
Ankle ligaments
Medial/Deltoid Ligament – attached to the medial malleolus; primary action is to resist over-eversion of the foot.
Lateral Ligament – comprised of three distinct and separate ligaments (anterior and posterior talofibular and calcaneofibular); resists over-inversion of the foot.
Subtalar Joint
An articulation between the talus and calcaneus.
the interosseous talocalcaneal ligament – acts to additionally bind the talus and calcaneus together
The joint is formed on an oblique axis and is therefore the chief site within the foot for generation of eversion and inversion movements
What are the arches of the foot?
- Medial longitudinal
- Lateral Longitudinal
- Anterior transverse arch
each are formed by different bones, but all supported by muscles, plantar ligaments, plantar aponeurosis
Greater Trochanter of Femur
= the most lateral palpable projection of bone; originates from the anterior aspect
Site of attachment for many of the muscles in the gluteal region – e.g. gluteus medius, gluteus minimus and piriformis.
The vastus lateralis originates from this site.
Lesser trochanter of femur
projects from the posteromedial side of the femur, just inferior to the neck-shaft junction.
It is the site of attachment for iliopsoas
Intertrochanteric line vs Intertrochanteric crest
LINE =
- anterior surface of the femur,
- site of attachment for the iliofemoral ligament
- anterior attachment of the hip joint capsule
CREST =
- posterior surface of the femur
Medial and lateral condyles of femur
The posterior and inferior surfaces articulate with the tibia and menisci of the knee
The anterior surface articulates with the patella.
Medial and lateral epicondyles of femur
= bony elevations on the non-articular areas of the condyles
medial and lateral collateral ligaments originate here
Patella - attachments
Connected inferiorly to tibial tuberosity via PATELLAR LIGAMENT
Connected superiorly to the QUADRICEPS TENDON
posterior surface of the patella articulates with the femur
Patella - functions
two main functions:
1. Leg extension – Enhances the leverage that the quadriceps tendon can exert on the femur, increasing the efficiency of the muscle.
- Protection – Protects the anterior aspect of the knee joint from physical trauma.
Fascia Lata
= a deep fascial investment of the musculature of the thigh.
It begins proximally around the iliac crest and inguinal ligament
It ends distal to the bony prominences of the tibia.
Formed of tensor fascia lata and Iliotibial Tract
Tensor Fascia Lata
= a gluteal muscle that acts as a flexor, abductor, and internal rotator of the hip.
It also has a role for tensing the fascia lata (hence its name)
originates from the iliac crest and inserts into the iliotibial tract
=> superior gluteal nerve innervation
Iliotibial Tract
= a longitudinal thickening of the fascia lata, which is strengthened by fibres from the gluteus maximus.
Acts as an extensor, abductor and lateral rotator of the hip, with an additional role in providing lateral stabilisation to the knee joint.
Superficial Gluteal Muscles
Gluteus Maximus
Gluteus Medius
Gluteus Minimus
Deep Gluteal Muscles
Piriformis
Obturator Internus
The Gemelli (superior and inferior)
Quadratus Femoris
Why is piriformis a key landmark in the gluteal region?
The superior gluteal nerve and vessels emerge into the gluteal region superiorly to the piriformis (and vice versa for the inferior gluteal nerve).
The sciatic nerve enters the gluteal region directly inferior to the piriformis
Basic musculature of the thigh
- Anterior – innervated by the femoral nerve (L2-L4); act to extend the leg at the knee joint.
- Medial – innervated by the obturator nerve, act to adduct the hip.
- Posterior – innervated by the sciatic nerve (L4-S3); act to extend at the hip, and flex at the knee.
Quadriceps Femoris muscles
Vastus Lateralis
Vastus Intermedius
Vastus Medius
Rectus Femoris
=> unite proximal to the knee and attach to the patella via the quadriceps tendon
Main extensor of the knee
All 4 muscles are innervated by the femoral nerve
Muscles of anterior compartment of thigh
Iliopsoas
Quadriceps Femoris
Sartorius
Pectineus
Muscles of medial compartment of thigh
Adductor Magnus
Adductor Longus
Adductor Brevis
Obturator Externus
Gracilis
Muscles of posterior compartment of thigh
Biceps Femoris
Semitendinosus
Semimembranosus
Muscles of anterior compartment of leg
Tibialis Anterior
Extensor Digitorum Longus
Extensor Hallucis Longus
Muscles of lateral compartment of leg
Fibularis Longus
Fibularis Brevis
Muscles of posterior compartment of leg
SUPERFICIAL
Gastrocnemius
Plantaris
Soleus
DEEP
Popliteus
Tibialis Posterior
Flexor Digitorum Longus
Flexor Hallucis Longus
ligament of head of femur
= only intracapsular ligament of hip joint
it encloses a branch of the obturator artery (artery to head of femur), a minor source of arterial supply to the hip joint.
Articulations of the knee joint
- Tibiofemoral – medial and lateral condyles of the femur articulate with the tibial condyles.
=> It is the weight-bearing component of the knee joint. - Patellofemoral – anterior aspect of the distal femur articulates with the patella.
=> It allows the tendon of the quadriceps femoris (knee extensor) to be inserted directly over the knee – increasing the efficiency of the muscle.
ACL
= Anterior cruciate ligament
attaches at the anterior intercondylar region of the tibia where it blends with the medial meniscus.
It ascends posteriorly to attach to the femur in the intercondylar fossa.
PREVENTS ANTERIOR DISLOCATION
PCL
= Posterior cruciate ligament
attaches at the posterior intercondylar region of the tibia
ascends anteriorly to attach to the anteromedial femoral condyle.
It prevents posterior dislocation
Tibiofibular Joints
PROXIMAL
= an articulation between the head of the fibula and the lateral condyle of the tibia.
DISTAL
= an articulation between the fibular notch of the distal tibia and the fibula.
A fibrous joint, where the joint surfaces are by bound by tough, fibrous tissue.
Glenohumeral Joint
Articulation of humeral head with glenoid fossa of scapula
Acromioclavicular joint
Articulation of the clavicle with the acromion of the scapula
Infraspinous fossa
= the area below the spine of the scapula,
the infraspinatus muscle originates from this area.
Supraspinous fossa
= the area above the spine of the scapula;
the supraspinatus muscle originates from this area
greater tuberosity of humerus
located laterally on the humerus
It serves as an attachment site for three of the rotator cuff muscles – supraspinatus, infraspinatus and teres minor
lesser tuberosity of humerus
much smaller, and more medially located
It provides attachment for the last rotator cuff muscle – the subscapularis.
What is important about the surgical neck of humerus?
The axillary nerve and circumflex humeral vessels lie against the bone here
=> important to test for in a fracture there
What lies in the radial (or spiral) groove ?
The radial nerve and profunda brachii artery
Functions of the forearm bones
Ulna = stabilising bone
Radius = pivots to produce movement
Articulations of the ulna
Proximally, the ulna articulates with the trochlea of the humerus at the elbow joint.
Proximal Radio-ulnar joint
Distal radio-ulnar joint.
Articulations of the radius
Elbow joint – partly formed by an articulation between the head of the radius, and the capitulum of the humerus.
Proximal radioulnar joint – an articulation between the radial head, and the radial notch of the ulna.
Wrist joint – an articulation between the distal end of the radius and the carpal bones.
Distal radioulnar joint – an articulation between the ulnar notch and the head of the ulna.
What are the intrinsic muscles of the shoulder?
Deltoid
Teres Major
Supraspinatus
Infraspinatus
Teres Minor
Subscapularis
What are the muscles of the anterior compartment of the arm?
What is their innervation?
Biceps Brachii
Brachioradialis
Coracobrachialis
=> They are all innervated by the musculocutaneous nerve.
What are the muscles of the posterior compartment of the arm?
What is their innervation?
Triceps Brachii
Radial nerve.
What are the muscles of the anterior compartment of forearm?
• SUPERFICIAL: flexor carpi ulnaris, palmaris longus, flexor carpi radialis, pronator teres.
• INTERMEDIATE: flexor digitorum superficialis.
• DEEP: flexor pollicis longus, flexor digitorum profundus and pronator quadratus.
What is the innervation of the muscles of the anterior compartment of forearm?
They are mostly innervated by the median nerve
(except for the flexor carpi ulnaris and medial half of flexor digitorum profundus, which are innervated by the ulnar nerve).
What are the muscles of the posterior compartment of forearm?
SUPERFICIAL -
Brachioradialis;
Extensor Carpi Radialis Longus and Brevis
Extensor Digitorum Communis
Extensor Digiti Minimi
Extensor Carpi Ulnaris
DEEP
Supinator
APL
EPB
EPL
Extensor Indicis Proprius
What muscle tendons form the borders of the anatomical snuffbox?
APL + EPB = lateral border
EPL = medial border
Axillary Nerve
Nerve roots – C5 and C6.
SENSORY – Gives rise to the upper lateral cutaneous nerve of arm, which innervates the skin over the lower deltoid (‘regimental badge area’).
MOTOR – Innervates the teres minor and deltoid muscles
Musculocutaneous Nerve
Nerve roots – C5-C7
MOTOR – muscles in the anterior compartment of the arm (BBC).
SENSORY – gives rise to the lateral cutaneous nerve of forearm, which innervates the lateral aspect of the forearm.
Median Nerve
Nerve roots – C6 - T1 (also contains fibres from C5 in some individuals).
MOTOR:
- Innervates the flexor and pronator muscles in the anterior compartment of the forearm (except the flexor carpi ulnaris and part of the FDP)
- Also supplies innervation to the thenar muscles and lateral two lumbricals in the hand.
SENSORY:
- Palmar cutaneous branch innervates the lateral aspect of the palm,
- Digital cutaneous branch innervates the lateral three and a half fingers on the anterior (palmar) surface of the hand
Radial Nerve
Nerve roots – C5-T1.
SENSORY – Innervates most of the skin of the posterior forearm, the lateral aspect of the dorsum of the hand, and the dorsal surface of the lateral three and a half digits.
MOTOR – Innervates the triceps brachii and the extensor muscles in the forearm
Ulnar Nerve
Spinal roots – C8-T1.
It passes posterior to the elbow through the cubital tunnel.
It enters the hand via the ulnar canal (Guyon’s canal).
MOTOR:
- Two muscles of the anterior forearm - flexor carpi ulnaris and medial half of flexor digitorum profundus
- Intrinsic muscles of the hand (apart from the thenar muscles and two lateral lumbricals)
SENSORY
Medial one and half fingers and the associated palm area.
What is a positive McMurray’s Test?
Indicates a meniscus tear
=> pain, snapping / clicking/ locking = positive
Internal rotation of the tibia + Varus stress = lateral meniscus
External Rotation of the tibia + Valgus stress = medial meniscus
The defect is in which protein in Marfan’s?
Fibrillin-1
The defect is in which protein in Ehler Danlos?
Collagen
Gait Cycle
- Heel strike
- Foot flat,
- Mid stance,
- Toe off
- Swing
WALKING
=> the swing phase accounts for 40% of the cycle.
=> brief double stance phase when both feet are in contact with the ground.
RUNNING
=> includes a flight phase when neither foot is in contact with the ground.
How many incisions are needed in a lower leg fasciotomy for compartment syndrome?
there are 4 compartments, but only 2 incisions are needed
What are the 4A’s of ankylosing spondylitis?
Apical fibrosis
Anterior uveitis
Aortic valve incompetence
Achilles tendonitis
