UNIVERSITY

OF DUNDEE ORTHOPAEDIC STUDY GUIDE

Mr David Nicoll MBChB MD FRCSEd (Tr&Orth)

Contributors: Jamie Morrison, Jun Lim

Contents
Introduction ..................................................................................................................................................... 6

How to use this guide ................................................................................................................. 6

Pathology .......................................................................................................................................................... 8

Arthritis ........................................................................................................................................... 8
Osteoarthritis (OA) ................................................................................................................................ 8
Inflammatory arthropathies .............................................................................................................. 9
Orthopaedic infections ............................................................................................................ 13
Osteomyelitis ........................................................................................................................................ 13
Septic Arthritis ..................................................................................................................................... 15
Infection of Orthopaedic Surgical Implants ............................................................................. 15
Biochemical disorders of bone ............................................................................................. 16
Osteoporosis ......................................................................................................................................... 16
Osteomalacia & rickets ..................................................................................................................... 17
Hyperparathyroidism ........................................................................................................................ 18
Renal osteodystrophy ....................................................................................................................... 19
Pagets disease ...................................................................................................................................... 19
Genetic disorders of the musculoskeletal system ......................................................... 20
Osteogenesis imperfecta .................................................................................................................. 20
Skeletal Dysplasias ............................................................................................................................. 21
Connective Tissue Disorders .......................................................................................................... 21
Muscular Dystrophies ....................................................................................................................... 23
Congentital & Developmental disorders ........................................................................... 23
Limb malformations........................................................................................................................... 23
Developmental Dysplasia of the Hip (DDH) ............................................................................. 24
Talipes Equinovarus (Clubfoot) .................................................................................................... 24
Obstetric Brachial Plexus Palsy ..................................................................................................... 24
Disorders of knee alignment .......................................................................................................... 25
Neuromuscular disorders ...................................................................................................... 25
Cerebral Palsy ....................................................................................................................................... 25
Spina Bifida ............................................................................................................................................ 26
Polio .......................................................................................................................................................... 27
Other diseases of muscle......................................................................................................... 27
Osteochondritis and Avascular Necrosis (AVN) ............................................................. 28
Osteochondritis .................................................................................................................................... 29
AVN ........................................................................................................................................................... 29
Bone Tumours ............................................................................................................................ 30
Benign bone tumours ........................................................................................................................ 30
Malignant bone tumours .................................................................................................................. 31
Soft tissue tumours ................................................................................................................... 34
Benign soft tissue tumours ............................................................................................................. 34
Other musculoskeletal soft tissue swellings ............................................................................ 35
Malignant soft tissue tumours ....................................................................................................... 35

Elective Surgery ........................................................................................................................................... 37

Surgical strategies for the management of an arthritic joint .................................... 37

Arthroplasty / Joint Replacement ................................................................................................ 37
Excision or resection arthroplasty ............................................................................................... 39
Arthrodesis ............................................................................................................................................ 39
Osteotomy .............................................................................................................................................. 39
Soft tissue problems ................................................................................................................. 40
Surgery for joint instability .................................................................................................... 41
Correction of deformity ........................................................................................................... 41

Nerve decompression .............................................................................................................. 42

Joint contractures ...................................................................................................................... 42
Infection ........................................................................................................................................ 42
Tumours ........................................................................................................................................ 42
Paediatric Orthopaedics ........................................................................................................................... 43

Normal developmental milestones ..................................................................................... 43

Normal lower limb development and common variations ......................................... 44
Disorders of knee alignment .......................................................................................................... 44
Intoeing .................................................................................................................................................. 45
Flat feet .................................................................................................................................................... 45
Curly toes ................................................................................................................................................ 46
Paediatric hip problems .......................................................................................................... 46
Developmental Dysplasia of the Hip (DDH) ............................................................................. 46
Transient synovitis of the hip ........................................................................................................ 47
Perthes ..................................................................................................................................................... 47
SUFE Slipped Upper Femoral Epiphysis ................................................................................ 48
Paediatric & Adolescent knee problems ........................................................................... 48
Extensor mechanism problems ..................................................................................................... 49
Adolescent knee pain ......................................................................................................................... 49
Patellar instability ............................................................................................................................... 49
Osteochondritis dissecans (OCD) ................................................................................................. 50
Meniscal problems .............................................................................................................................. 50
Paediatric foot & ankle problems ........................................................................................ 50
Talipes Equinovarus (Clubfoot) .................................................................................................... 50
Tarsal coalition ..................................................................................................................................... 51
Hallux valgus ......................................................................................................................................... 51
Paediatric / Adolescent spine problems ........................................................................... 51
Scoliosis ................................................................................................................................................... 51
Spondylolisthesis ................................................................................................................................ 52

Adult Regional Orthopaedics ................................................................................................................... 53

Lumbar Spine .............................................................................................................................. 53

Mechanical Back Pain ........................................................................................................................ 53
Acute disc tear / Discogenic back pain ....................................................................................... 53
Sciatica / Lumbar Radiculopathy ................................................................................................. 53
Bony root entrapment ....................................................................................................................... 55
Spinal stenosis and spinal claudication ..................................................................................... 55
Osteoporotic crush fractures .......................................................................................................... 55
Cauda equina syndrome ................................................................................................................... 55
Red Flag symptoms & signs ............................................................................................................ 56
Neck ................................................................................................................................................ 56
Cervical spondylosis .......................................................................................................................... 56
Cervical disc prolapse ........................................................................................................................ 56
Cervical spine instability .................................................................................................................. 57
Shoulder ........................................................................................................................................ 58
Impingement syndrome / Painful arc syndrome................................................................... 59
Frozen shoulder (adhesive capsulitis) ....................................................................................... 60
Instability................................................................................................................................................ 60
Acute calcific tendonitis ................................................................................................................... 61
Other causes of shoulder pain ....................................................................................................... 61
Compressive Neuropathies .................................................................................................... 62
Carpal Tunnel syndrome .................................................................................................................. 62
Cubital Tunnel Syndrome ................................................................................................................ 62
Elbow .............................................................................................................................................. 64

Tennis Elbow Lateral epicondylitis .......................................................................................... 64

Golfers elbow Medial epicondylitis ......................................................................................... 64
Arthriticelbow ...................................................................................................................................... 64
Hands ............................................................................................................................................. 65
Dupytrens Contracture ..................................................................................................................... 65
Trigger Finger ....................................................................................................................................... 65
OA hand & wrist ................................................................................................................................... 66
RA hands ................................................................................................................................................. 66
Ganglion cyst ......................................................................................................................................... 67
Giant cell tumour of tendon sheath ............................................................................................. 68
Hip ................................................................................................................................................... 69
Hip Arthritis & Total Hip Replacement (THR) ........................................................................ 69
AVN of the hip ....................................................................................................................................... 70
Trochanteric bursitis / gluteal cuff syndrome ........................................................................ 70
Knee ................................................................................................................................................ 71
Knee arthritis and Knee replacement ......................................................................................... 71
Soft tissue injuries of the knee ....................................................................................................... 72
Osteochondral and chondral injuries ......................................................................................... 75
Extensor mechanism ruptures ...................................................................................................... 75
Patellofemoral dysfunction ............................................................................................................. 75
Patellar instability ............................................................................................................................... 76
Foot and Ankle ............................................................................................................................ 77
Ankle OA arthrodesis and replacement ................................................................................. 77
Hallux Valgus ........................................................................................................................................ 77
Hallux rigidus 1st MTPJ OA ........................................................................................................... 78
Mortons Neuroma .............................................................................................................................. 78
Stress fracture ...................................................................................................................................... 79
Achilles Tendonitis and Rupture .................................................................................................. 79
Plantar fasciitis ..................................................................................................................................... 79
Flat foot ................................................................................................................................................... 80
Pes cavus ................................................................................................................................................. 80
Claw and hammer toes ..................................................................................................................... 81
Trauma ........................................................................................................................................................... 82

Management of Major Trauma ............................................................................................. 82

Primary survey ..................................................................................................................................... 82
Secondary Survey ................................................................................................................................ 85
Polytrauma and Damage Control Orthopaedics ..................................................................... 85
The fracture process and fracture healing ....................................................................... 87
Fracture patterns ................................................................................................................................ 88
Describing a fracture ......................................................................................................................... 88
Childrens fractures ............................................................................................................................ 90
Clinical signs of a fracture ................................................................................................................ 92
Investigation of a fracture ............................................................................................................... 92
Complications of fractures .............................................................................................................. 92
Assessment of an injured limb ....................................................................................................... 98
Initial management of a long bone fracture ............................................................................. 98
Definitive fracture management ................................................................................................... 99
Signs of fracture healing and nonunion ................................................................................... 99
Dislocations & Instability .................................................................................................... 100
Soft tissue injury ..................................................................................................................... 100
Regional Trauma .................................................................................................................... 102
Spine ....................................................................................................................................................... 102
Pelvis ...................................................................................................................................................... 107

Acetabular fractures ........................................................................................................................ 109

Shoulder ................................................................................................................................................ 109
Humeral shaft fracture .................................................................................................................... 111
Elbow ..................................................................................................................................................... 111
Forearm fractures ............................................................................................................................. 112
Distal radius fractures ..................................................................................................................... 113
Scaphoid & carpus ............................................................................................................................ 114
Hand Trauma ...................................................................................................................................... 115
Hip ........................................................................................................................................................... 116
Femoral shaft fracture .................................................................................................................... 117
Knee ........................................................................................................................................................ 117
Tibial shaft fracture .......................................................................................................................... 119
Distal tibia & Pilon fractures ........................................................................................................ 120
Ankle ....................................................................................................................................................... 120
Foot ......................................................................................................................................................... 121
Common childrens fractures ....................................................................................................... 122

Introduction

Howtousethisguide

This study guide covers the orthopaedic syllabus for undergraduates. Although some information
is provided on rheumatological conditions, this is from an orthopaedic / surgical perspective as
many rheumatological conditions may present to the orthopaedic clinic as an outpatient or may
be present to the acute orthopaedic service. For more detailed information regarding the
diagnosis and medical management of the common rheumatological conditions, please refer to
rheumatology lectures and recommended texts.

Orthopaedics is predominantly taught during the 2nd year teaching programme with a clinical
attachment in 4th year. As neurology and neurosciences are not covered in detail until 3rd year,
musculoskeletal conditions with neurologic sequelae are not considered core knowledge for 2nd
year students, but are for 4th year students. Similarly the management of major trauma and
intensive care aspects of trauma management are reserved for 4th year students.

Expected core knowledge for 2nd year students is detailed in this study guide as unhighlighted
text.

Further coreknowledge expected of 4th year students is highlighted in lilac.

Further reading for those who strive for merit/distinction or for junior doctors or General
Practitioners with an interest in orthopaedics is highlighted in grey.

Orthopaedics literally means straight children and refers to the historical workload of
orthopaedic surgeons who dealt with deformity due to congenital or developmental
abnormalities of the skeleton. Fortunately such abnormalities are now far less common and the
work of an Orthopaedic surgeon now covers a huge range of diseases affecting the
musculoskeletal system covering all age ranges.

Orthopaedics involves extensive knowledge of anatomy including musculoskeletal gross
anatomy and microscopic anatomy. Students are also expected to have reasonable knowledge of
physiological and biochemical processes as well as an understanding of pathological conditions
of the musculoskeletal system.

The study of anatomy is outwith the purpose of this study guide but nevertheless thorough
knowledge of the names of bones of the axial and appendicular skeleton as well as the names of
various tuberosities, condyles and parts of bones is essential. Knowledge of the actions, origins,
insertions and nerve supplies of the various skeletal muscles in their distinct fascial
compartments is also essential, as is a thorough understanding of the peripheral nervous system.

The following is a list of basic science topics which students should also have a thorough
understanding of:

Microscopic structure of cortical (compact) and cancellous (spongy) bone
Types of joints and structure of a typical synovial joint
Microcopic anatomy of hyaline cartilage
Microscopic anatomy of the physis (growth plate)
Microscopic organization of skeletal muscle and the sarcomere
Microscopic organization of tendons and ligaments
Biochemistry of bone and calcium homeostasis
Physiology of nerve conduction, the neuromuscular junction, muscle contraction and
reflexes
Energy production, catabolism and cellular respiration
Fracture healing
Skin and soft tissue healing

Nerve healing
Embryologic development of the musculoskeletal system
Normal growth and development
Basic genetics

Please note this list is not exhaustive.

The aim of this guide is to discuss the more common orthopaedic pathological processes of the
musculoskeletal system with regards to their aetiology, presentation and management. In the UK
the specialty of Orthopaedics also encompasses Trauma surgery which involves the management
of fractures and dislocations as well as the general management of the trauma / multiply injured
patient.

Thus Orthopaedics can be separated into cold or elective conditions which do not usually
necessitate emergency management and traumatic or infective disorders which may require
urgent or emergency management.

Firstly, common pathological conditions of the musculoskeletal system will be discussed
followed by a synopsis of the common nontraumatic and traumatic conditions of the various
anatomic regions.

Pathology
Arthritis

The treatment of arthritic conditions provides the mainstay of elective orthopaedic surgical
practice with, in particular, hip and knee replacement two of the most commonly performed and
successful surgical procedures. The term arthropathy is used to describe a disease of the joint
whereas arthritis describes inflammation of the joint. Both expressions are often used
synonymously.

The two main categories of arthritis are:

Osteoarthritis (OA)
Inflammatory arthritis

Additionally inflammatory arthritis can be further subdivided into:

Rheumatoid arthritis
Seronegative inflammatory arthropathy (many different types)

Osteoarthritis(OA)

OA is by far the most common form of arthritis and is primarily a degenerative disorder. Over
time the normal structure of every joint is subject to wear and deterioration. Alongside OA there
may also be a considerable amount of associated inflammation, which can lead to periodic flaring
of the OA.

Despite the prevalence of OA we still have very little understanding of the definitive underlying
mechanism. However, it is generally accepted that an imbalance exists between wear and repair
of cartilage within joints. There may be a familial link but no pattern of Mendelian inheritance
exists and no formal genetic mutation has been identified. Environmental factors, hobbies and
type of work may have an influence and joints with abnormal alignment (developmental or
pathological) are at higher risk of OA. Previous injuries (articular cartilage injuries, intra
articular fractures, extraarticular fractures with subsequent malalignment, meniscal injuries)
can also give rise to secondary OA. Often, however, no definite causative factor is found (known
as primary OA)

Some causes of 2 OA are listed:

Congenital dislocation of the hip
Perthes
SUFE
Previous intraarticular fracture
Extraarticular fracture with malunion
Osteochondral / hyaline cartilage injury
Crystal arthropathy
Inflammatory arthritis (can give rise to mixed pattern arthritis)
Meniscal tears
Genu Varum or Valgum

InterpretationofaXrayinosteoarthritis

The following are typical radiographic findings of an osteoarthritic joint:



L loss of joint space


O osteophytes




S sclerosis


S subchondral cysts

Image of hip and knee with OA with findings identified

The difficulty with imaging of joints in older age groups is matching investigation findings with
symptoms. It can be the case that some patients with substantial Xray changes of OA have minimal
symptoms. The converse is also true some patients who are substantially symptomatic can have
only mild disease on imaging. Hence the most important learning point we can take from this is that
in orthopaedics you treat the patient and their symptoms and not the images.

Inflammatoryarthropathies

The diagnosis and treatment of inflammatory arthropathies is covered in rheumatology. Presented
here is a summary of the musculoskeletal manifestations of the common rheumatological conditions
and their potential surgical management.

Inflammatory arthropathies can be classified into four broad groups seropositive, seronegative,
infectious and crystal deposition disorders.

Many of the inflammatory arthropathies are due to an autoimmune mediated conditions where
the patients own immune system attacks the joints and sometimes the connective tissues of the
musculosketal (and other) system(s). These conditions can give a wide array of systemic
manifestations. The mainstay of treatment is pharmacological with simple analgesia, anti
inflammatory medications (steroids & NSAIDs), steroid injections and Disease Modifying Anti
Rheumatoid Drugs (DMARDs). The rheumatology component of the musculoskeletal teaching
block will provide more information regarding the pathology and treatment of the various
inflammatory arthropathies and basic information only is provided here.

RheumatoidArthritis

Rheumatoid arthritis is the most prevalent seropositive inflammatory arthropathy although
around 15% of patients with the disease are negative for serological Rheumatoid factor.

Rheumatoid arthritis is an autoimmune inflammatory symmetric polyarthropathy which most
commonly affects the small joints of the hands and feet as well as the cervical spine. Larger joints
such as the hips, knees, shoulders and elbows can also be affected. Women are 23 times more
commonly affected than men. Identified autoantibodies which can be measured and aid
diagnosis include Rheumatoid Factor and AntiCCP. CRP and ESR are usually raised. Diagnosis is
based on the clinical presentation, radiographic findings and serological analysis. The
ACR/EULAR Rheumatoid Arthritis Criteria scoring system assists in the diagnosis.

In the disease process, an immune response is initiated against synovium which lines synovial
joints and some tendons. An inflammatory pannus forms which then attacks and denudes
articular cartilage leading to joint destruction. Tendon ruptures and soft tissue damage can occur
leading to joint instability and subluxation. Clinical features include synovitis (doughy swelling),
pain, morning stiffness, deformity (see hands section) and loss of function. Cutaneous
rheumatoid nodules can occur and internal organs can also be affected (rheumatoid lung,
Ischaemic Heart Disease).

Xrays tend to show a hypotrophic artritis (rather than the hypertrophic picture with OA) with
loss of joint space but little or no osteophyte formation, sclerosis or bone cysts. Instead
periarticular erosions occur.

Treatment is aimed at pain relief, reducing the number of flareups and maintaining function.
With the advent of newer DMARDs, the number of rheumatoid arthritis sufferers requiring
surgery has markedly reduced in recent times. Physiotherapists, occupational therapists,
podiatrists and orthotists can also have an important role. Surgery can be used for resistant
disease, to control pain from a particular joint or to improve or maintain function. Operations
performed for rheumatoid arthritis include:

Synovectomy
Joint replacement
Joint excision
Tendon transfers
Arthrodesis (fusion)
Cervical spine stabilisation

SystemicLupusErythematosis

Joint involvement can occur in patients with SLE with a predilection for the hands and knees.
Avascular necrosis can also occur in the hip and knee and tendon ruptures can also occur. Again
pharmacological agents to relieve pain and suppress the immune system are the mainstay of
treatment with surgery for tendon ruptures and severe symptomatic joint damage
SeronegativeAutoImmuneInflammatoryArthropathies

Seronegative inflammatory arthropathies have many common features with several distinct
subtypes. They often have inflammation and/or arthritic disease of the spine where they are
known as Spondyloarthropathies. Sacroiliitis, uveitis and dactylitis (inflammation of a digit) are
also common. Patients usually have an asymmetric oligoarthritis, enthesopathies are common
(especially achilles insertional tendonitis and plantar fasciitis) and patients are often HLAB27
positive on serological testing (although only a minority of HLAB27 positive patients develop a
spondyloarthritis). CRP and ESR are usually elevated.

Ankylosing spondylitis is a chronic inflammatory disease of the spine and sacroiliac joints
which leads to eventual fusion of the intervertebral joints and SI joints. Males are more

10

commonly affected (3:1) and age of onset is typically between 2040 years. Patients complain of
pain and stiffness and they may also develop knee or hip arthritis. Associated conditions include
aortitis, pulmonary fibrosis and amyloidosis. Xrays show bony spurs from the vertebral bodies
known as syndesmophytes which can bridge the intervertebral disc resulting in fusion producing
a bamboo spine. 90% of sufferers are HLAB27 positive. Treatment consists of physiotherapy,
exercise, simple analgesia and DMARDs for more aggressive disease. Surgery is mainly reserved
for hip and knee arthritis and Kyphoplasy to straighten out the spine is controversial and carries
considerable risk.

Psoriatic arthritis occurs in up to 30% of people affected by skin psoriasis. Again the arthritis is
usually asymmetrical oligoarthritis and sacroiliitis, spondylitis, dactylitis and enthesitis
commonly occur. Patients usually have nail changes including pitting and onycholysis (lifting of
the nail from its nailbed). Some patients have a predilection for arthritis of the DIP joints of the
fingers and/or toes and 5% of patients have a particularly aggressive and destructive form of the
condition known as arthritis mutilans. Again treatment is mainly pharmacological with DMARDs
inreaingly used to control disease. Joint replacement can be considered in larger joints which are
severely affected and DIP joint fusion can help.

Enteropathic arthritis refers to an inflammatory arthritis involving the spine and peripheral
joints occurring in patients with inflammatory bowel disease (Crohns disease and Ulcerative
Colitis), coeliac disease, patients with extensive bowel resections and patients with a reactive
arthritis from bacterial or parasitic infection of the GI tract (Shigella, Salmonella, Yersinia,
Campylobacter, Cryptosporidium, Giardia and others). 1020% of IBD sufferers will experience
spine or joint problems. Treatment includes treating the underlying condition (corticosteroids,
antibiotics) and DMARDs can help. Any peripheral arthritis is usually selflimiting and
orthopaedic surgery is not required but steroid injection can help.

Reactive arthritis occurs in response to an infection in another part of the body, most
commonly GI infections (as above) or genitourinary infections (Chlamydia, Neisseria). Large
joints eg the knee become inflamed around 13 weeks following the infection. The infection
triggers an autoimmune arthropathy. Some patients have a triad of symptoms of urethritis,
uveitis and arthritis known as Reiters syndrome. Most cases are selflimiting whilst others (15
30%) are chronic or have frequent relapses. Treatment is aimed at the underlying infectious
cause, symptomatic relief and occasionally DMARDs are required.

Figure 1: Joint involvement in different types of arthritis. Source: Douglas G et al. (2009)

CrystalArthropathy

11

Gout is a crystal arthropathy caused by deposition of urate crystals within a joint which is
usually due to high serum uric acid levels (hyperuricaemia). Uric acid is the final compound in
the breakdown of purines in DNA metabolism (adenine & guanine). Hyperuricaemia may be due
to renal underexcretion (which can be exacerbated by diuretics or renal failure) or due to
excessive intake of alcohol, red meat and seafood. There is also some evidence for a genetic
predisposition. Uric acid crystal form in joints and can be triggered by dehydration, trauma or
surgery. Chemotherapy agents can also cause the disease. Although any joint can be affected the
first metatarsalphalangeal (MTP) joint is the classic site of disease (known as Podagra) with the
ankle and knee the other most commonly affected joints. Gout presents with an intensely painful
red, hot swollen joint which may mimic a septic arthritis. Gouty tophi which are painless white
accumulations of uric acid can occur in the soft tissues and erupt through the skin. Chronic gout
can result in a destructive erosive arthritis.

A definitive diagnosis can be made by analysing a sample of synovial fluid with polarised
microscopy (the fluid is also analysed with Gram stain and culture to exclude infection). Uric acid
crystals are needle shaped and display negative birefringence (change from yellow to blue when
lined across the direction of polarization).

Treatment for acute attacks includes NSAIDs, corticosteroids, opioid analgesics and colchicine for
patients who cannot tolerate NSAIDs (though it can have GI side effects and interfere with other
medications). For sufferers of recurrent attacks or those with joint destruction or tophi,
allopurinol or probenecid can prevent attacks but they should not be started until an acute attack
has settles as theoretically they could potentiate an acute attack.

Pseudogout is another crystal arthropathy causing an acute arthritis but in contrast to gout, it is
caused by calcium pyrophosphate crystals. The term chondrocalcinosis is used when calcium
pyrophosphate deposition occurs in cartilage and other soft tissues in the absence of acute
inflammation. Both come under the umbrella of Calcium Pyrophosphate Deposition (CPPD).
CPPD tends to affect the knee, wrist and ankle. The exact cause is unknown and it can coexist
with hyperparathyroidism, hypothyroidism, renal osteodystrophy, haemochromatosis and
Wilsons disease. It can also occur in some cases of OA however chronic CPPD can also result in
osteoarthritic change. Treatment of acute attacks includes NSAIDs, corticosteroids (systemic and
intraarticular) and occasionally colchicine. There are no medications used as prophylaxis to
prevent recurrence.

Figure 2: A) Positively birefringent crystals of calcium pyrophosphate dihydrate (CPPD). (B)
Negatively birefringent crystal of monosodium urate monohydrate. Source: Luqmani R et al.
(2013)

12

Orthopaedicinfections

Orthopaedics may be involved in the management of soft tissue infections (infected bursitis, arm
or leg abscesses, wound infections) which may require surgery, particularly if an abscess is
present. The mainstay of this section, however, is to discuss bone and joint infection.
Osteomyelitis
Osteomyelitis means infection of bone including compact and spongy bone as well as the bone
marrow. Infection is usually caused by bacteria and is occasionally fungal. Organisms can infect
bone directly by penetrating trauma or surgery or indirectly by haematogenous spread form an
infection or bacteraemia at a distant site (eg area of cellulitis). Any infection depends on the
bacterial load inoculated, the virulence of the organism and the hosts immune defences.
Immunocompromised patients, those with chronic disease, the elderly, and the young are most
prone to osteomyelitis.
Once infected, enzymes from leucocytes cause local osteolysis and pus forms which impairs local
blood flow making the infection very difficult to eradicate. A dead fragment of bone known as a
sequestrum can form which usually breaks off and once a sequestrum is present, antibiotics
alone will not cure the infection. New bone will form around the area of necrosis known as an
involucrum. Additionally Staph. aureus can infect osteocytes intracellularly making infection
additionally difficult for the immune system to reach.
An acute osteomyelitis in the absence of recent surgery usually occurs in children, however
immunocompromised adults can also be affected.
In children, the metaphyses of long bones contain abundant tortuous vessels with sluggish flow
which can result in accumulation of bacteria and infection spreads towards the epiphysis. In
neonates and infants, certain metaphyses are intraarticular including the proximal femur,
proximal humerus, radial head and ankle and infection can spread into the joint causing co
existent septic arthritis. Additionally, infants have loosely applied periosteum and an abscess can
extend widely along the subperiosteal space. Children can also develop a subacute osteomyelitis
with a more insidious onset and where the bone reacts by walling off the abscess with a thin rim
of sclerotic bone. This is known as a Brodies abscess.
Chronic osteomyelitis develops from an untreated acute osteomyelitis and may be associated
with a sequestrum and/or involucrum. In adults the infection tends to be in the axial skeleton
(spine or pelvis) with haematogenous spread from pulmonary or urinary infections, or from
infection of the intervertebral disc (discitis). Chronic OM in children or adults can be peripheral
from previous open fracture or internal fixation. Chronic OM can be suppressed with antibiotics
and can lay dormant for many years before reactivating causing localized pain, inflammation,
systemic upset and possible sinus formation. Tuberculosis can also cause chronic OM,
particularly in the spine through haematogenous spread from the primary lung infection.
Causative organisms for various age groups are demonstrated in the table below (note that a
mixed picture may exist:

13


Newborns (younger than 4 mo)

S. aureus, Enterobacter sp., and group A & B Strep

Children (aged 4 mo to 4 y)
S. aureus, group A Strep, Haemophilus influenzae
(reduced with Hib vaccine), and Enterobacter sp.

Children, adolescents (4y to S. aureus (80%), group A Strep, H. influenzae, and
adult)
Enterobacter sp.

Adult
S. aureus and occasionally Enterobacter or Streptococcus
sp

Sickle cell anaemia patients
S. aureus the most common, but Salmonella species are
common and fairly unique to sickle cell patients


Osteomyelitis can be classified as being superficial (affecting the outer surface of bone),
medullary, localized (affecting cortex and medullary bone) or diffuse (where a segment of bone is
infected resulting in skeletal instability eg infected nonunion).
Acute osteomyelitis is usually treated by best guess antibiotics intravenously unless there is
abscess formation which mandates surgical drainage. If the infection fails to resolve, second line
antibiotics may be used or surgery may be performed to gain samples for culture, remove
infected bone and washout the infected area.
Chronic osteomyelitis cannot be cured or eradicated by antibiotics alone. Active infection can be
suppressed with antibiotics but this may prove unsuccessful. Surgery is usually recommended to
gain deep bone tissue cultures, to remove any sequestrum and to excise any infected or non
viable bone (known as debridement). Note that samples from any discharging sinus may not
accurately reflect the organism causing the deep infection. If debridement of bone results in
instability, the bone must be stabilized by internal or external fixation. The advantage of external
fixation is that the bone can be subsequently lengthened if it has been shortened as a result of the
debridement. Other strategies may include local antibiotic delivery systems and bone grafting.
Plastic surgery may be required if skin and soft tissue coverage of bone is not possible.
Intravenous antibiotics are continued for several weeks after surgery.
Poorly controlled diabetics, intravenous drug abusers and other immunocompromised patients
are at particular risk of osteomyelitis of the spine. Osteomyelitis can also complicate spinal
surgery. The lumbar spine is the commonest location but anywhere in the spine can be involved.
Patients present with insidious onset of back pain which is constant and unremitting. They have
paraspinal muscle spasm and spinal tenderness and may have fever and/or systemic upset.
Severe cases may have an associated neurologic deficit (lower motor neurone & cauda equina
syndrome below L1 and upper motor neurone / myelopathy above L1). Pus may extrude forming
a paravertebral or epidural abscess. As the vertebral end plates weaken, vertebrae may collapse
leading to kyphosis or vertebra plana (flat vertebra) and disc space may reduce. MRI delineates
the extent of the infection and any abscess formation. Blood cultures may indicate the causative
organism (usually Staph. aureus including MRSA but atypical infections can occur in the
immunocompromised). Endocarditis should be considered (look for clubbing, splinter
haemorrhages, murmur, consider ECHO).
Treatment consists of high dose IV antibiotics after CT guided biopsy to obtain tissue culture.
Antibiotics may be required for several months and response is assessed clinically and by serial
CRP. Around half of all patients go on to spontaneous fusion and resolution. Indications for
surgery include inability to obtain cultures by needle biopsy, no response to antibiotic therapy,
progressive vertebral collapse and progressive neurological deficit. Surgery involves
debridement, stabilization and fusion of adjacent vertebrae.

14

SepticArthritis

Acute onset of a severely painful red, hot, swollen and tender joint with severe pain on any
movement are the typical presenting features of a septic arthritis. In most cases the offending
pathogens spread to the joint via the blood or from an infection of adjacent tissues. In some cases
there will be a history of direct penetration of a joint with a sharp object (eg a fight bite wound
from a punching injury and penetration of a tooth or a rose thorn injury from gardening). Septic
arthritis can also occur following intraarticular surgery.

Although septic arthritis is relatively uncommon in adults, such is the importance of early
detection and intervention that it should be excluded with any unexplained acute monoarthritis.
Bacterial infections can irreversibly damage hyaline articular cartilage within days and therefore
septic arthritis is considered an emergency to try to avoid chronic arthritic damage. Similar to
osteomyelitis the young, elderly, IVDUs and immunocompromised patients are most prone to
infection. As mentioned previously, neonates and infants have some intracapsular metaphyses
and septic arthritis can evolve in some joints from metaphyseal osteomyelitis. Again endocarditis
should be looked for if suspected particularly if more than one joint or bone is involved (due to
septic emboli).

Bacteria that are commonly found to cause septic arthritis include:
Staphylococcus aureus the most common cause in adults
Streptococci the second most common cause
Haemophilus influenzae was the most common cause in children but is now uncommon
in areas where Haemophilus vaccination is practiced
Neisseria gonorrhoea in young adults (now thought rare in Western Europe)
Escherichia coli in the elderly, IV drug users and the seriously ill

Any joint suspected of septic arthritis should be aspirated under aseptic technique before
antibiotics are given to confirm the diagnosis and to identify the causative organism such that
appropriate antibiotic therapy can be targeted at the responsible bacteria. A single dose of
antibiotics can lead to a falsely negative Gram stain and culture.

If frank pus is aspirated, the clinical picture fits with obvious septic arthritis or a positive Gram
stain is found, the treatment is usually surgical washout either via open surgery or using
arthroscopic techniques. Some clinicians practice repeat aspirations along with intravenous
antibiotic therapy rather than surgical washout with some evidence to support this, particularly
in children. Open washout however is probably the best technique to decrease the bacterial load
throughout the joint. Response to treatment is based on clinical findings and serial CRP.
InfectionofOrthopaedicSurgicalImplants

Any operative intervention carries a small risk of subsequent infection. Common orthopaedic
implants include joint replacements for arthritic conditions (and occasionally for instability and
tumour surgery) whilst for fracture fixation and skeletal stabilization pins, wires, plates, screws,
intramedullary nails and external fixators are used.

Despite improved infection rates with strict antisepsis, sterilisation of implants and instruments,
special air flow theatres and perioperative antibiotics, unfortunately it seems that surgical site
infection cannot be completely eradicated with a deep infection risk of around 12% for non
contaminated orthoapedic procedures. Bacteria can enter the operative site at the time of
surgery (usually from the patients own skin and bacteria buried deep within the hair follicles
which antiseptics cant reach or from shed skin cells from staff in theatre) or they can enter the
wound postoperatively before it has healed. Haematoma in the soft tissues can act as a very
effective culture medium for bacteria to thrive on. Bacteria can also infect a prosthetic joint at a
later stage by haematogenous spread.

When a deep infection complicates a prosthetic joint replacement, the concern is development of
chronic infection with pain, poor function, recurrent sepsis, chronic discharging sinus formation
and implant loosening. When a deep infection complicates a fracture fixation or stabilization,

15

there is a risk of chronic osteomyelitis and nonunion of the fracture. As you will see later in the
trauma and joint replacement sections, deep infections in orthopaedics can lead to substantial
disability which is why orthopaedic surgeons and nursing staff are so strict about antisepsis in
theatre and on the wards.

Common virulent organisms which produce an early prosthetic infection include Staph. aureus
and gram negative bacilli including coliforms. Some organisms cause a more indolent or low
grade infection which is inevitably diagnosed late (up to a year after surgery) and often requires
surgical intervention. Such bacteria include Staph. epidermidis (also known as coagulase negative
staphylococci) and enterococcus. Organisms associated with late onset haemotogenous infection
Include Staph. aureus, beta haemolytic Streptococcus and Enterobacter.

For any orthopaedic infection, the solution is usually surgical rather than treating with
antibiotics. Antibiotics should not be given until a decision regarding surgery has been made,
even for seemingly superficial wound infections, as any antibiotics can interfere with the
bacteriological tissue cultures and the causative organism may not be identified from surgical
debridement.

Prosthetic joint (joint replacement) infection: see later

Fracture stabilization infection: see later

Biochemicaldisordersofbone
Osteoporosis

Osteoporosis is a quantitative defect of bone characterised by reduced bone mineral density and
increased porosity (i.e. the bone is of normal quality, there is just not enough of it). This leads to
fragility of the bone and increased fracture risk with fractures occurring after little or no trauma.
The WHO defines osteoporosis as bone mineral density less than 2.5 standard deviations below
the mean peak value of young adults of the same race and sex. Osteopenia is an intermediate
stage where bone mineral density is between 1 to 2.5 standard deviations below mean peak
value.

Figure 3: Comparison of normal bone and osteoporotic bone. Source: Staker B (2013)

Loss of bone mineral density is for the most part a physiologic phenomenon which starts at
around the age of 30 with a very gradual slowdown in osteoblastic activity. Females tend to lose
more bone mineral density after the menopause due to an increase in osteoclastic bone
resorption with the loss of protective effects of oestrogen.

Two types of primary osteoporosis have been described. Type 1 is known as PostMenopausal
Osteoporosis with an exacerbated loss of bone in the postmenopausal period. Early menopaiuse
may have an influence whilst familial and environmental factors (white Caucasians at particular

16

risk) may play a role. Further risk factors include smoking, alcohol abuse, lack of exercise and
poor diet. Colles fractures and vertebral insufficiency fractures tend to occur in this group. Type
2 is known as Osteoporosis of old age with a greater decline in bone mineral density than
expected. Risk factors are similar with the added risks of chronic disease, inactivity and reduced
sunlight exposure (Vitamin D). Femoral neck fractures and vertebral fractures predominate in
this group. Osteoporosis can also occur secondary to other conditions including corticosteroid
use, alcohol abuse, malnutrition, chronic disease (CKD, malignancy, Rheumatoid arthritis) and
endocrine disorders (Cushings, Hyperthyroidism, Hyperparathyroidism).

Diagnosis is by way of DEXA scanning to provide a measure of bone mineral density, and values
are compared with standard peak values for race and sex as well as age standardized values.
Serum calcium and phosphate are normal.

Unfortunately once osteoporosis is diagnosed, no treatments can increase bone mineral density.
Treatments aim to slow any further deterioration and hopefully decrease the risk of subsequent
fracture. Building up peak bone mineral density by way of exercise, good diet and healthy levels
of sunlight exposure before bone density starts to decline may reduce the risk of osteoporosis
and it is also important to try to maintain exercise and a healthy lifestyle. Pharamcological
treatments used to try to prevent fragility fractures include calcium and vitamin D supplements
(if dietary intake is poor), bisphosphonates (alendronate, risedronate, etidronate) which reduce
osteoclastic resorption, Desunomab (a monoclonal antibody which reduces osteoclast activity)
and strontium (which increases osteoblast replication and reduces resorption). Zoledronic acid is
a once yearly intravenous bisphosphonate but is substantially more expensive than oral forms.

Intranasal Calcitonin has been tried but no benefit over other treatments has been found and its
use is associated with a small increased cancer risk.

HRT is not recommended as a first line agent for the prevention of osteoporosis after the
menopause however can be considered if side effects with other medications occur. Risks include
increased breast and endometrial cancer rates and DVT. Raloxifene (an oestrogen receptor
modulator) can also be considered but again there is a risk of DVT.

Some of these medications can have side effects and at present oral bisphosphonates have the
greatest evidence for efficacy, costeffectiveness and low side effect profile.

Osteomalacia&rickets

Osteomalacia is a qualitative defect of bone with abnormal softening of the bone due to deficient
mineralization of osteoid (immature bone) secondary to inadequate amounts of calcium and
phosphorus. Rickets is the same disease occurring in children which has subsequent effects on
the growing skeleton.

The principal causes of osteomalacia and rickets involve either insufficient calcium absorption
from the intestine because of lack of dietary calcium or a deficiency of or resistance to the action
of vitamin D; or phosphate deficiency caused by increased renal losses. Specific causes include
malnutrition (Ca & vit D), malabsorption (low vit D absorption), lack of sunlight exposure (no
activation vit D), hypophosphateamia (refeeding syndrome, alcohol abuse impairs phosphate
absorption, malabsorption, renal tubular acidosis), long term anticonvulsant use and chronic
kidney disease (reduced phosphate resorption & failure of activation vitamin D). Some renal
diseases are inherited disorders (Xlinked hypophosphataemia or vitamin D resistant rickets)

Patients may complain of bone pain (pelvis, spine and femora), have deformities from soft bones
(particularly rickets), sustain pathological fractures easily and have symptoms of hypocalcaemia
(paraesthesiae, muscle cramps, irritability, fatigue, seizures, brittle nails). Radiographs may also
demonstrate pseudofractures (aka Loosers zones) particularly of the pubic rami, proximal
femora, ulna and ribs.

17

In contrast to osteoporosis serum bone biochemistry is abnormal with typically a low calcium,
low serum phosphate and high serum alkaline phosphatase.

Treatment involves vitamin D therapy with calcium and phosphate supplementation.

Figure 4: Deformities in child with rickets. Source: Dandy D and Edwards DJ (2009).

Hyperparathyroidism

Figure 5: Parathyroid regulation of calcium homeostasis. Source: Taniegra ED (2004)

Hyperparathyroidism involves overactivity of the parathyroid glands with high levels of
parathyroid hormone (PTH).

Primary hyperparathyroidism is due to a benign adenoma, hyperplasia or rarely a malignant
neoplasia. Overproduction of PTH results in hypercalcaemia with subsequent symptoms and

18

signs (fatigue, depression, bone pain, myalgia, nausea, thirst, polyuria, renal stones,
osteoporosis). Serum PTH is usually elevated and calcium is high. Phosphate is normal or low.

Secondary hyperparathyroidism is a physiological overproduction of PTH secondary to
hypocalcaemia usually caused by vitamin D deficiency or CKD.

Tertiary hyperparathyroidism is seen in patients with chronic secondary hyperparathyroidism
(usually CKD) who develop an adenoma which will continue to produce PTH despite biochemical
correction.

Hyperparathyroidism can result in fragility fractures and can also cause lytic lesions in bone
(known as Brown Tumours or osteitis fibrosa cystica) which may need skeletal stabilization.
Treatment of hyperparathyroidism includes removal of the adenomatous gland or treatment of
the underlying cause (vitamin D supplementation). Very high serum calcium levels need
emergency treatment (iv fluids, bisphosphonates, calcitonin).

Renalosteodystrophy

This describes the typical bone changes due to CKD. Reduced phosphate excretion and inactive
activation of vitamin D results in secondary hyperparathyroidism with subsequent osteomalacia,
sclerosis of bone and calcification of soft tissues.
Pagetsdisease

Pagets disease of bone is a chronic disorder which results in thickened, brittle and misshapen
bones. Typically it affects only one or a few bones and it affects approximately 4% of over 55 year
olds and up to 10% of over 80s. Viral infection (paramyxoviruses) and genetic defects have been
implicated in the aetiology. Increased osteoclast activity (possibly due to an exaggerated
response to vitamin D) results in increased bone turnover. Osteoblasts become more active to try
to correct excessive bone resorption. The osteoblasts form new bone however the new bone fails
to remodel sufficiently and the resulting bone despite its increased thickness and bone density is
brittle and can fracture easily.

Figure 6: Crosssection of femur of Paget's disease, characterised by cortical thickening and
deformity. Source: Underwood JCE (2009)

19

Bones commonly affected include the pelvis, femur, skull, tibia and sometimes the ear ossicles
(resulting in conductive deafness).

Pagets disease of the bone can be asymptomatic and present as an incidental finding on Xray. It
can also cause arthritis (if close to the joint), pathologic fractures, deformity, pain and high
output cardiac failure (due to increased blood flow through pagetic bone).

Serum alkaline phosphatase is raised whilst calcium and phosphorus are usually normal.
Radiographic features demonstrate that the affected bone is enlarged with thickened cortices
and coarse, thickened trabeculae with mixed areas of lysis and sclerosis. Bone scans demonstrate
marked increased uptake in the affected bone(s).

Treatment is with bisphosphonates (which inhibit osteoclasts) or calcitonin if extensive lytic
disease. Joint replacement may be necessary and pathological femoral fractures should be
stabilized with long intramedullary nails or plates.

Geneticdisordersofthemusculoskeletalsystem
Osteogenesisimperfecta

Also known colloquially as brittle bone disease, osteogenesis imperfect is a defect of the
maturation and organization of type 1 collagen (which accounts for most of the organic
composition of bone). The majority of cases are autosomal dominant with multiple fragility
fractures of childhood, short stature with multiple deformities, blue sclerae and loss of hearing.
Rarer cases are autosomal recessive and are either fatal in the perinatal period or associated
with spinal deformity.

Figure 7: Wholebody images of adults with osteogenesis imperfecta with the use of dualenergy
xray absorptiometry. Note that most adults have scoliosis. Source: Reeder J and Orwoll E (2006).

20


Figure 8: Blue sclerae in Osteogenesis Imperfecta. Source: LeidigBruckner G and Grauer A
(1998)

Multiple fractures can be mistaken for child abuse / NonAccidental Injury (NAI). Osteopenia can
also result from prematurity and result in low energy fractures. Thorough but sensitive history
and examination.

Bones tend to be thin (gracile) with thin cortices and osteopenic. Mild cases may have relatively
normal xrays with history of low energy fractures.

Fractures tend to heal with abundant but poor quality callus and are treated with splintage,
traction or surgical stabilization. Some cases develop progressive deformity which may require
multiple osteotomies and intramedullary stabilization for correction (Sofield procedure).
SkeletalDysplasias

Skeletal dysplasia is the medical term for short stature (dwarfism is no longer used) and is due to
genetic error (hereditary or sporadic mutation) resulting in abnormal development of bone and
connective tissue. Short stature may be proportionate (limbs and spine proportionally short) or
disproportionate (limbs propotionally shorter or longer than spine). More than 300 types of
skeletal dysplasia have been described.

The commonest and most recognized type is achondroplasia which may be autosomal dominant,
however over 80% of cases are sporadic. Achondroplasia results in disproportionately short
limbs with a prominent forehead and widened nose. Joints are lax and mental development is
normal.

Other skeletal dysplasias can be associated with learning difficulties, spine deformity, limb
deformity, internal organ dysfunction, craniofacial abnormalities, skin abnormalities, tumour
formation (especially haemangiomas), joint hypermobility, atlantoaxial subluxation, spinal cord
compression (myelopathy) and intrauterine or premature death.

Genetic testing of the child and family should be considered and orthopaedic treatment
comprises of deformity correction (including severe scoliosis correction) and limb lengthening.
Growth hormona therapy may be appropriate.
ConnectiveTissueDisorders

These are due to genetic disorders of collagen synthesis (mainly type 1 found in bone, tendon
and ligaments) resulting in joint hypermobility. Osteogenesis imperfecta predominantly affects
the type 1 collagen of bone whereas the connective tissue disorders affect soft tissues more than
bone.
Generalised(Familial)jointlaxity

21

Around 5% of normal people have hypermobility of the joints which usually runs in families and
is inherited in a dominant manner. Patients may describe themselves as doublejointed and be
able to perform tricks as a party piece (eg voluntary dislocation of the shoulder).

People with generalized ligamentous laxity are more prone to soft tissue injuries (ankle sprains)
and recurrent dislocations of joints (especially shoulder and patella) which may be painful.
Marfanssyndrome

Marfans syndrome is an autosomal dominant or sporadic mutation of the fibrillin gene resulting
in tall stature with disproportionately long limbs and ligamentous laxity. Associated features
include a high arched palate, scoiliosis, flattening of the chest (pectus excavatum), eye problems
(lens dislocation, retinal detachment), aortic aneurysm and cardiac valve incompetence. Cardiac
abnormalities may result in premature death.

Patients rarely require orthoapedic surgery (scoliosis and bony procedures for joint instability
eg fusions) and soft tissue stabilization of dislocating joints usually has disappointing results as
the biological abnormality cannot be corrected.

Figure 9: Sign's of Marfan's syndrome. Source: Kumar P and Clark M (2012)

EhlersDanlossyndrome

This is a heterogeneous condition which is often autosomal dominantly inherited with abnormal
elastin and collagen formation. More than 10 types have been described. Clinical features include
profound joint hypermobility, vascular fragility with ease of bruising, joint instability and
scoliosis. Bony surgery may be required for dislocating joints however bleeding can be a problem
and skin healing can be poor with stretched scars or wound dehiscence common.
Downsyndrome

Musculoskeletal manifestations of Trisomy 21 include short stature and joint laxity with possible
recurrent dislocation (especially patella) which may require stabilization. Atlantoaxial
instability in the cspine can also occur (see later)

22

MuscularDystrophies

These are rare and usually Xlinked recessive hereditary disorders (therefore only affecting
boys) resulting in progressive muscle weakness and wasting.

Duchennemusculardystrophy

A defect in the dystrophin gene involved in calcium transport results in muscle weakness which
may only be noticed when the boy starts to walk with difficulty standing (see Gowers sign
below) and going up stairs. Progressive muscle weakness follows and by the age of 10 or so he
can no longer walk and by age 20 progressive cardiac and respiratory failure develop with death
typically in the early 20s.

Diagnosis is confirmed by raised serum creatinine phosphokinase and abnormalities on muscle
biopsy. Physiotherapy, splintage and deformity correction may prolong mobility. Severe scoliosis
may be corrected by spinal surgery.

Figure 10: Gower's sign, classically seen in Duchenne muscular dystrophy. Source: Douglas G et
al. (2009).

Beckersmusculardystrophy

This is similar to DMD but milder with affected boys able to walk in their teens and sufferers may
survive into their 30s or 40s.

Congentital&Developmentaldisorders
Limbmalformations

Limb malformations include extra bones, absent bones, short (hypoplastic) bones and fusions of
bones and/or skin and soft tissues. Some are genetically determined with an autosomal
dominant inheritance whilst others are due to an insult to the developing limb bud usually
between the 4th and 6th weeks of gestation. Some limb malformations may be associated with
genetically inherited syndromes.

Syndactyly is the commonest congenital malformation of the limbs where two digits (fingers or
toes) are fused due to failure of separation of the skin/soft tissues or phalanges of adjacent digits
either partially or along the entire length of the digits. Surgical separation may be required
(usually at age 3 or 4).

Polydactyly is where an extra digit is formed and can be treated by amputating the extra digit.

23

Fibular hemimelia is one of the most common limb deficiencies which involves partial or
complete absence of the fibula often with absence of the lateral foot rays leading to a shortened
limb, bowing of the tibia and ankle deformity. Mild cases can be treated with limb lengthening
with a circular frame external fixator whilst more severe cases are best treated with a through
ankle amputation at 10 months to 2 years old and use of a below knee prosthetic limb.

Other causes of congenital leg length inequality of the lower limbs include deficiencies of the
proximal femur and tibia. Absence or hypoplasia of the radius in the upper limb leads to
underdevelopment of the hand (usually absence of the thumb) with marked deformity (radial
club hand). Surgical reconstruction may be required with thumb reconstruction from the index
ray (pollicisation) and correction of the deformity.

Congenital fusions can occur with the most common being a fusion between two of the tarsal
bones of the foot (known as tarsal coalition) which may case painful flat feet in later childhood.
The abnormal connection may need surgically divided.

DevelopmentalDysplasiaoftheHip(DDH)

See Paediatric Orthopaedics section
TalipesEquinovarus(Clubfoot)

See Paediatric Orthopaedics section
ObstetricBrachialPlexusPalsy

The incidence of brachial plexus injury during vaginal delivery is around 2 in 1000 and most
commonly arises in large babies (macrosomia in diabetes), twin deliveries and shoulder dystocia
(difficult delivery of the shoulder after the head with compression of the shoulder on the pubic
symphysis).

The commonest type is Erbs palsy with injury to the upper (C5 & C6) nerve roots resulting in
loss of motor innervation of the deltoid, supraspinatus, infraspinatus, biceps and brachilais
muscles. This leads to internal rotation of the humerus (from unopposed subscapularis) and may
lead to the classic waiters tip posture. Physiotherapy is required to prevent contractures early
on and prognosis is predicted by the return of biceps function by 6 months with good outcome in
8090% of cases. Surgical release of contractures and tendon transfers may be required if no
recovery.

Figure 12: Characteristic position of the upper extremity in Erbs palsy. Source: Douglas G et al.
(2009)

24



Klumpkes palsy is much rarer and is a lower brachial plexus injury (C8 &T1 roots) caused by
forceful adduction which results in paralysis of the intrinsic hand muscles +/ finger and wrist
flexors and possible Horners syndrome (due to disruption of the first sympathetic ganglion from
T1). The fingers are typically flexed (due to paralysis of the interossei and lubricals which assist
extension at the PIP joints). The prognosis is poorer than for Erbs palsy with less than 50%
recovery and there is no specific treatment.

Figure 11: Characteristic position of the upper extremity in Klumpkes palsy. Source: Pediatric
Orthopedics (2010)

Total brachial plexus palsy after birth carries the poorest prognosis

Disordersofkneealignment

See Paediatric Orthopaedics section

Neuromusculardisorders

Neuromuscular disorders occur due to abnormal or deficient motor neuron signals to skeletal
muscle due to a defect in either the brain, spinal cord, peripheral nerve, neuromuscular junction
or muscle. There are many, many causes of neuromuscular disease with only the most common
presented here. Upper motor neuron (UMN brain and spinal cord) causes give rise to weakness,
spasticity (rate dependant increased tone), hyperreflexia and an extensor plantar response
(Babinski sign). Lower motor neuron (LMN affecting anterior horn cells, nerve roots or
peripheral nerve) causes result in weakness, reduced tone and hypo or areflexia.

There are many different neuromuscular disorders however only the main causes which may
involve orthopaedics will be discussed here.

CerebralPalsy

Cerebral Palsy (CP) is a neuromuscular disorder with onset before 23 years of age due to an
insult to the immature brain before, during or after birth. Causes include genetic problems, brain
malformation, intrauterine infection in early pregnancy, prematurity, intracranial haemorrhage,
hypoxia during birth and meningitis. Only 1 in 10 cases are due to problems during labour
(contrary to popular belief) whilst often there is no identifiable cause or explanation. The
expression of the disease and its severity are variable depending on the area of the brain affected
ranging from mild symptoms and signs limited to one limb or total body involvement with
profound learning difficulties. Developmental milestones may be missed and the ability to
ambulate or perform normal tasks may be impaired.

25

The commonest expression of CP is spastic CP occurring in 80% of cases with injury to the motor
cortex, upper motor neurons or corticospinal tract resulting in weakness and spasticity which
may worsen as the child grows. Other types include Ataxic (which affects the cerebellum) which
reduces coordination and balance and Athetoid (affecting the extrapyramidal motor system, the
pyramidal tract and basal ganglia) which results in an uncontrolled writhing motion, sudden
changes in tone and difficulties controlling speech. CP can affect one limb (monoplegic), one
ipsilateral upper and lower limb (hemiplegic the most common), both legs only (diplegic) and
all 4 limbs usually with learning difficulties (total body involvement). Developmental milestones
may be delayed in young children.

Figure 14: Cerebral palsy can be classified according to distribution, physiologic type or
neurological substrate. Source: Miller MD (2012).


Musculoskeletal problems which can develop include joint contractures, scoliosis and hip
dislocation (noncongenital). Nonsurgical treatment for CP includes physiotherapy and splintage
(orthotics) to prevent contractures, the medicine baclofen (which can be given by injection
intrathecally in the subarachnoid space to allow a lower dose and fewer side effects) to reduce
spasticity and Botox injection into spastic muscles. Surgical treatments include hip excision or
replacement to treat painful hip dislocation and subsequent problems with wheelchair sitting,
surgical release of joint contractures, correction of severe scoliosis, joint fusions and tendon
transfers. Some cases of spasticity can be helped by the spinal procedure of selective dorsal
rhizotomy which involves sectioning of overfiring motor nerve rootlets chosen by intraoperative
EMG however the long term benefit is not fully known, complications can be severe and it is only
performed in a few specialist centres.
SpinaBifida

Spina bifida is a congenital disorder where the two halves of the posterior vertebral arch fail to
fuse, probably in the first six weeks of gestation.

In its mildest form known as spina bifida occulta, there may be no associated problems but some
can develop tethering of the spinal cord and roots which can cause a high arched foot (pes cavus)
and clawing of the toes. Neurological symptoms however can occur at any age. Some have a tell
tale dimple or tuft of hair in the skin overlying the defect.

In its more severe form, spina bifida cystica, the contents of the vertebral canal herniate through
the defect with either hernmiation of the meninges alone (a meningocele) or with the spinal cord
or cauda equina. A meningocele is not usually associated with neurological sequelae but a
myelomeningocle usually has a neurological deficit (motor and sensory) below the lesion and
most will never function independently. Spina bifida cystica may be associated with

26

hydrocephalus (excess CSF around the brain raising intracranial pressure) and the degree of
disability depends on the spinal level affected.

Figure 15: Types of Spina Bifida. Source: Yale Medical Group ()

With spina bifida cystica the defect is usually closed with 48 hours of birth (to prevent drying or
infection). Hydrocephalus may be treated with a shunt from the ventricles of the brain to either
the right atrium, pleural cavity or peritoneal cavity at a few weeks of age. Spinal deformity and
hip dislocation are also common and contractures can occur.

Orthopaedic surgical management includes scoliosis correction, reduction and containment
procedures for the hip, contracture released and correction of foot deformities. Avoidance of
pressure sores and good foot care is important to prevent ulcers and sores which can get
infected.
Polio

Polio (or poliomyelitis) is a viral infection affection motor anterior horn cells in the spinal cord or
brainstem resulting in a lower motor neurone deficit. Vaccination has eradicated new cases of
polio in modern healthcare systems however older patients with long term effects of childhood
polio are occasionally encountered.

The virus enters via the GI tract with a flulike illness and a variable degree of paralysis usually
affecting a group of muscles of one limb within 23 days. Some affected motor neurons recover
with recovery of weakness however residual paralysis can occur. Joint deformities and growth
defects can occur with shortening of the limb. Sensation is preserved.

Treatment of residual paralysis can be treated with splintage (caliper, orthotics) and shortening
of a leg can be helped with a shoe raise. Tendon transfers may improve function whilst some
deformities especially of the foot or ankle can be treated with fusion (arthrodesis) to provide a
better platform for ambulation. Flail joints may also be treated with arthrodesis in a position of
maximal function and shortening can be treated with lengthening of the short side or shortening
of the long side.

Otherdiseasesofmuscle

Polymyalgia Rheumatica is a condition mainly seen in middle aged and elderly women
resulting in aching pain around the shoulder and pelvic girdles with stiffness and weakness. It is

27

due to a giant cell arteritis and patients may develop temporal arteritis which can result in
blindness if untreated. ESR is very high and treatment involves oral corticosteroids.

Fibromyaligia is a chronic pain condition with widespread pain characterized by allodynia a
heightened pain response to pressure. Painful pressure points around the neck, shoulders, trunk
and limbs have been decribed. The pathology is unclear causing many to doubt its existence a
true medical condition and it is unclear if it should be classified as a musculoskeletal condition or
neuropsychiatric disorder. Fatigue, sleep disturbance, numbness and paraesthesiae often coexist.
There are no diagnostic tests and pharmacologic treatments include analgesics, muscle relaxants,
antidepressants, antiepileptics and dopamine agonists. Fibromyalgia is usually a predictor of
poor outcome after orthopaedic surgery.

Figure 16: Pressure point in fibromyalgia. Source: Kumar P and Clark M (2012)

Polymyositis is an inflammatory disorder affecting muscles of the shoulder and hip regions
whose cause is not fully known. Evidence suggests it may be an autoimmune disease, viruses
have been implicated and cancer can trigger the disease. Pain and weakness ensue. Serum CK is
elevated, electromyographs (EMG) have abnormal patterns and muscle biopsy demonstrated the
inflammatory process. It is related to the skin condition dermatomyositis.

Myositis ossificans is a condition where heterotopic ossification (bone forming outside the
skeleton) occurs in muscles usually after an injury. The injury may be innocuous and it can form
after muscle contusion (dead leg), fractures (especially around the elbow) and dislocations
(especially traumatic hip dislocation). Heterotopic ossification can also occur in the muscles and
soft tissues after surgery including hip replacement particularly if it is a revision (redo)
procedure. Bony masses are seen in the soft tissues on xray. Stiffness may develop but aggressive
physiotherapy may result in more ectopic bone formation making the situation worse. Once the
new bone formation has settled, the abnormal bone can be excised to try to relieve stiffness with
high strength NSAIDs (Indomethacin) or radiotherapy used to help prevent recurrence.

OsteochondritisandAvascularNecrosis(AVN)

Osteochondritis and AVN have a similar end result in that an area of bone undergoes localized
necrosis as a result of ischaemia from a reduction in blood supply.

28

Osteochondritis

Osteochondritis tends to occur in children and young adults and may be due to increased
physical activity with repetitive stress (compression or traction). There may be a familial
predisposition whilst some cases may have an underlying coagulopathy. (Recurrent) Impact or
traction injuries cause bleeding and oedema within the bone, resulting in capillary compression.
Bone necrosis ensues resulting in compression, fragmentation or separation of bone (and
overlying cartilage if intraarticular) which may cause flattening and incongruence of a joint or a
pothole on the surface. Pain and progression to arthritis at a young age if a joint is involved may
follow.

Common sites affected by compression include the 2nd metatarsal head (known as Freiburgs
disease), the navicular bone (known as Kohlers disease), the lunate of the carpus (known as
Kienbocks disease and the capitellum of the elbow (known as Panners disease). Vertebral
compression can also occur (Scheuermanns disease). Perthes disease of the hip (see later) is also
thought to be a compression osteochondritis affecting the developing hip. Traction
osteochondritis occurs at an apophysis (a bony tubercle where a tendon attaches) including the
tibial tubercle (known as Osgood Schlatter disease) and the calcaneus (known as Severs
disease).

Fragmentation with separation of bone and cartilage within a joint is known as osteochondritis
dissecans. Certain sites are particularly predisposed (lateral part of medial femoral condyle in
the knee, anteromedial talar done, superomedial femoral head and the humeral capitellum). Pain
and effusions ensue and locking can occur with giving way of weight bearing joints.

Perthes disease is discussed in the childrens orthopaedics section. Compression types of
osteochondritis may settle with few or no ongoing problems. Restriction of activities may be
enough and splintage may help in the wrist or foot. However in more severe cases arthritis in
affected or neighbouring joints can occur. Traction osteochondritis is selflimiting and settles
with rest.

If joint is damaged from osteochondritis, osteotomy (surgical realignment of a bone ) can shift
the load in a joint from a damaged area to an undamaged area (especially knee or Freiburgs
disease). Osteochondritis dissecans can be treated by pinning of unstable fragments or removal
of detached fragments. Larger defects increase the risk of progression to arthritis.

AVN

AVN is an ischaemic necrosis of bone predominantly in adults. Several sites are particularly
prone to AVN including the femoral head, the femoral condyles, the head of the humerus, the
capitellum, the proximal pole of the scaphoid and the proximal part of the talus.

AVN can be secondary to fractures of the femoral neck, proximal humerus, waist of scaphoid and
talar neck where the fracture disrupts the blood supply to an entire portion of bone. Many cases
of AVN are idiopathic where no cause is found however AVN can also be due to alcoholism and
steroid (ab)use which are two of the commonest identifiable causes found. Alcoholism and
corticosteroids alter fat metabolism which can result in mobilization of fat into the circulation
which can sludge up the capillary system and promote coagulation within prone areas of bones
and the increased fat content of the marrow can compress venous outflow from the bone causing
stasis and ischaemia. Primary hyperlipidaemia can also result in AVN in the same way.

AVN can also be due to thrombophilia, sickle cell diease and antiphospholipid deficiency in SLE
which all serve to increase coagulability.

A rare cause is Caissons disease or decompression sickness which causes AVN from nitrogen gas
bubbles forming in the circulation after too rapid a depressurization after deep sea diving.

29

AVN results in necrosis of a segment of bone resulting in patchy sclerosis before subchondral
collapse and irregularity of the articular surface occurs. Secondary OA ensues.

AVN can also secondarily affect osteoarthritic joints causing collapse of the articular surface and
rapid deterioration. The mechanism for this is unclear however it can be impossible to determine
if the AVN came first and resulted in secondary osteoarthritis or if the OA came first and was
complicated by AVN.

Treatment of AVN depends on the stage of the disease. Early cases can be seen on MRI before any
radiographic changes occur. If the articular surface has not collapsed in an amenable site (usually
the femoral head) drilling can be performed under fluoroscopy to decompress the bone,
prevent further necrosis and help healing. If the articular surface has collapsed generally joint
replacement is usually required in the hip, knee or shoulder to control symptoms. Fusion can be
considered in the wrist or foot/ankle.

BoneTumours
Benignbonetumours

Benign bone tumours (which dont metastasize) can be neoplastic, developmental, traumatic,
infectious or inflammatory in nature.

The commonest is an osteochondroma which produces a bony outgrowth on the external surface
with a cartilaginous cap. These do not usually case any problems but can produce local pain.
There is a very small (1%) risk of malignant transformation and any lesion growing in size or
producing pain may require excisional biopsy. Multiple osteochondromata can occur as an
autosomal dominant hereditary disorder.

An enchondroma is an intramedullary and usually metaphyseal cartilaginous tumour caused by
failure of normal enchondral ossification at the growth plate. The lesion is usually lucent but can
undergo mineralization with a patchy sclerotic appearance. Many are incidental findings and the
lesions are usually asymptomatic but can weaken the bone resulting in pathologic fracture.
Endchondromas can occur in the femur, humerus, tibia and small bones of the hand and feet.
Once a fracture has healed or if there is a risk of impending fracture they may be scraped out
(curettage) and filled with bone graft to strengthen the bone.

A simple bone cyst (aka unicameral bone cyst) is a single cavity benign fluid filled cyst in a bone.
They are probably a growth defect from the physis and are therefore metaphyseal in long bones
(usually in the proximal humerus and femur) although they can occur in the talus or calcaneus.
They may be asymptomatic and an incidental finding on xray (usually a child or young adult)
however they can cause weakness leading to pathological fracture. Again treatment with
curettage and bone grafting with or without stabilization may be required.

An aneurysmal bone cyst in contrast contains lots of chambers which are filled with blood or
serum. The different chambers may be seen on xray. They are thought to be due to a small
arteriovenous malformation. They can occur in the metaphyses of many different long bones, flat
bones (ribs, skull) and vertebral bodies. The lesion is locally aggressive causing cortical
expansion and destruction and is usually painful. Again there is a risk of pathological fracture.
Treament is again with curettage and grafting or the use of bone cement.

A giant cell tumour of bone can also be locally aggressive and they also have a predilection for the
metaphyseal region but tend to involve the epiphysis and can extend to the subchondral bone
adjacent to the joint. GCTs most commonly occur around the knee and in the distal radius but can
occur in other long bones, the pelvis and the spine. They occur after the physis has fused and are
locally destructive destroying cortex. They are painful and may cause pathological fracture. The
aetiology is unknown but as the name suggests histologically they consist of mulinucleate giant
cells. On Xray they have a characteristic soap bubble appearance. Although they are considered
benign, 5% can metastasize to the lung with benign pulmonary GCT. Treatment is intralesional
excision with use of phenol, bone cement or liquid nitrogen to destroy remaining tumour

30

material and reduce the risk of recurrence. Very aggressive lesions with cortical destruction may
need joint replacement.

Fibrous dysplasia is a disease of a bone usually occurring in adolescence where a genetic
mutation results in lesions of fibrous tissue and immature bone. It can affect one bone
(monostotic) or more (polyostotic). Defective mineralization may result in angular deformities
and the affected bone is wider with thinned cortices. Stress fractures can occur. Extensive
involvement of the proximal femur can produce a shepherds crook deformity. Bone scans show
intense increase in uptake during development but the lesion usually becomes inactive.
Bisphosphonates may reduce pain and pathologic fractures should be stabilized with internal
fixation and cortical bone grafts used to improve strength. Simple intralesional excision alone has
a very high recurrence rate.

An osteoid osteoma is a small nidus of immature bone surrounded by an intense sclerotic halo.
They most commonly occur in adolescence and common sites include the proximal femur, the
disphysis of long bones and the vertebrae. The predominant clinical feature is intense constant
pain, worse at night due to the intense inflammatory response. This pain is greatly relieved by
NSAIDs. The lesion may be seen on xray however bone scan (intense local uptake) and CT can
confirm the diagnosis. The lesion may resolve spontaneously over time but some cases may
require CT guided radiofrequency ablation or en bloc excision.

A Brodies abscess (subacute osteomyelitis) and hyperparathyroidism (Brown tumours) can also
present with a lytic lesion of bone.
Malignantbonetumours

Malignant primary bone tumours are very rare when considered alongside other forms of
primary malignancy. On the other hand metastatic cancer affecting the skeleton is common.

Delayed diagnosis of primary or secondary bone tumour may adversely affect the patients
prognosis and result in undue pain. Certain red flags in history taking may arouse suspicion of
cancer of the bone. Cancer affecting bone tends to produce a constant pain which may be severe
and is usually worse at night. Systemic symptoms may also be present (weight loss, loss of
apetite, fatigue). Patients over age 60 are more likely to develop cancer and metastatic disease
and unexplained skeletal pains in this age group should be investigated. Similarly young patients
(less than around 20 years old) should not have unexplained skeletal pain and again
investigation is warranted to exclude neoplasia or infection to ensure an uncommon but
significant diagnosis is not missed.

Malignantprimarybonetumours

Malignant primary bone tumours can occur in young patients (although they can occur at any
age) and are not uncommonly misdiagnosed for muscular pains and presentation is often late in
the disease process and metastases may have occurred. Any red flags or any unexplained
persistent pain warrants investigation with at least an xray. Some primary bone tumours may
have a substantial illdefined bony swelling this finding mandates urgent investigation and
referral.

Malignant primary bone tumours show aggressive and destructive signs on xray including
cortical destruction, a periosteal reaction (raised periosteum producing bone), new bone
formation (sclerosis as well as lysis from destruction) and extension into the surrounding soft
tissue envelope.

The most common form of primary bone tumour is osteosarcoma, named according to the fact it
is a malignant tumour producing bone. Most cases are seen in younger age groups (adolescence
and early adulthood) with 60% involving the bones around the knee. Other sites include the
proximal femur, proximal humerus and pelvis. Metastatic spread is usually haematogenous but

31

can be lymphatic. 10% of patients have pulmonary metastases at diagnosis. Whilst they are not
radiosensitive, adjuctive chemotherapy can prolong survival.

Figure 12: The most common location of osteosarcoma (purple). The secondary locations of
osteosarcoma may commonly be found (blue). Source: Miller MD (2012).


Chondrosarcoma is a cartilage producing primary bone tumour and is less common and less
aggressive than osteosarcoma. It tends to occur in an older age group (mean age 45). They can
be very large and are slow to metastasize. They tend to be found in the pelvis or proximal femur.
The prognosis is dependant on the histological grade with the majority being low grade. They are
not radiosensitive and unresponsive to adjuvant chemotherapy thus far.

Fibrosarcoma and Malignant Fibrous Histiocytoma are fibrous malignant primary bone tumours
which tend to occur in abnormal bone (bone infarct, fibrous dysplasia, post irradiation, Pagets
disease). Fibrosarcona tends to affect adolescents or young adults.

Ewings sarcoma is a malignant tumour of endothelial cells in the marrow, It is the 2nd most
prevalent primary bone tumour and has the poorest prognosis. Most cases occur between the
ages of 10 and 20. It may be associated with fever, raised inflammatory markers and a warm
swelling and may be misdiagnosed as osteomyelitis. It tends to be radio and chemosensitive.

The treatment of primary bone tumours usually involves surgery to remove the tumour and
surrounding tissue to reduce the risk of recurrence. Amputations used to be more commonly
employed to minimize recurrence risk but with improved adjuvant therapy, limb salvage surgery
has equivalent success rates and better functional outcome, if appropriate. Staging investigations
usually include bone scan and CT chest. MRI and CT are useful to determine the local extent of
the tumour and the involvement of muscle, nerves and vessels. Biopsy is required for histological
diagnosis and grading prior to definitive surgery. In general the biopsy should normally be
performed in the specialist centre where definitive surgery is performed. Typically a bone
tumour is removed with a wide margin of 34cm of bone and a cuff of normal muscle all around.
The biopsy tract is also removed with the tumour. The joint involved needs reconstruction with
special joint replacements which are typically much bigger than standard replacements to
counteract the extensive bone loss.

Adjuvant chemotherapy and radiotherapy are used if appropriate and neoadjuvant
chemotherapy (given prior the surgery) can improve survival. Advances in adjuvant therapy
have improved the survival rates from primary bone tumours from around 50% to 80% 5 year
survival over the last few decades.

32

Lymphoma (a cancer of round cells of the reticuloendothelial system / macrophages) can occur
as a primary bone tumour (as Non Hodgkins Lymphoma) from the marrow or lymphoma (any
type) can metastasize to bone (in 20% of cases). Primary lymphoma of bone tends to affect the
pelvis or femur and treatment is with surgical resection. With metastatic lymphoma
lymphadenopathy or splenomegaly may be present and treatment is chemotherapy and
radiotherapy. Survival of metastatic lymphoma is usually less than 2 years.

Myeloma (a malignant B cell proliferation [antibodies]) arises from the marrow and can present
as a solitary lesion (known as a plasmacytoma) or with multiple osteolytic lesions throughout the
skeleton (known as multiple myeloma). Patients are typically aged 4565 and with multiple
myeloma have weakness, back pain, bone pain, fatigue, weight loss and may have marrow
suppression resulting in anaemia and recurrent infection. Patients may present with pathologic
fracture. Diagnosis is by plasma protein electrophoresis (showing a high level of paraprotein)
and early morning urine collection for Bence Jones protein assay. Note that with these lytic
lesions there is not usually an osteoblastic response to the osteoclastic bone resorption and
metastases may not be detected on bone scan. A skeletal survey of xrays is required. Treatment
of a solitary plasmacytoma is by radiotherapy whilst treatment of multiple myeloma is by
chemotherapy. 5 year survival is less than 30%.

Metastaticbonetumours

Primary malignant tumours which commonly metastasize to bone include (in order of
frequency):

Breast carcinoma

Prostate carcinoma
Lung carcinoma
Renal cell carcinoma

Thyroid adenocarcinoma

Other cancers tend not to metastasize to bone but infrequently do including adenocarcinoma of
the colon, bladder cancer and even melanoma.

Breast cancer bony metastases can be blastic (sclerotic) or lytic. Mean survival with bony
metastases is around 2426 months.

Prostate cancer commonly metastasizes to bone and produces sclerotic metastases. Because of
the osteoblastic activity pathologic fractures are more likely to heal. Radiotherapy and hormone
manipulation can reduce the fracture risk of a bone metastasis. Survival with prostatic bony
metastases is around 45% at one year.

Lung cancer usually gives rise to lytic bony metastases and once bone metastases are present,
mean survival is around 6 months.

Renal cell carcinoma usually gives rise to potentially large and very vascular lytic blow out
bony metastases which can bleed tremendously with biopsy or surgery. With a single bone
metastasis and a primary tumour amenable to resection (nephrectomy), surgery can potentially
be curative. Mean survival with multiple bone metastases is 1218 months.

Bones most frequently involved with metastases include the vertebra, pelvis, ribs, skull, humerus
and long bones of the lower limb. The pain may initially be misdiagnosed as a muscle strain
however any pain with red flags should be investigated at least with an xray initially. Patients
may also present with pathological fracture. If a lesion is found on xray, a primary bone tumour
must be excluded (by bone scan and occasionally MRI). Bone scan will also demonstrate the
extent of bone metastases. If there are multiple metastases or the lesion is suspected to be
metastatic, the primary tumour should be sought (there may be history of previously diagnosed
or treated primary). Examination may include breast exam or PR exam. CXR may detect a

33

pulmonary lesion. Blood tests include serum calcium (for hypercalcaemia), LFTs (to look for liver
mets), plasma protein electrophoresis (for myeloma), full blood count and U&E.

Lesions which are very painful (especially on weight bearing), those which occupy >50% of the
diameter of the bone, those with cortical thinning and those in at risk areas (eg subtrochanteic
area of the femur) may be at risk of impending pathological fracture and skeletal stabilization or
joint replacement may be required.

Fractures or impending fractures are treated with stabilization using long rods (intramedullary
nails) whilst if there is destruction of a joint (eg acetabulum or femoral head) the joint
replacement may be a better option. Surgery has a high risk of DVT and prophylaxis must be
given. Chemotherapy and radiotherapy may be given after surgery.

Painful lesions thought not to be at risk of impending fracture can be treated with
bisphosphonates and radiotherapy (if radiosensitive). Spinal cord compression can occur with
advanced spinal metastases and can be improved with radiotherapy or surgical decompression
(anterior or posterior).

Of course treatments are provided in response to the patients wishes and are influenced by the
patients symptoms and prognosis. Patients with advanced disease may only be suitable for
palliative care.

Softtissuetumours

A soft tissue swelling may present to orthopaedics if situated on an arm or leg. Soft tissue
swellings may be diffuse (as in synovitis or oedema) or local. Local swellings include
inflammatory swellings (bursitis, rheumatoid nosules), infection (abscess), cystic lesions
(ganglion, meniscal cyst, Bakers cyst), benign neoplasms and malignant neoplasms.

The usual history taking for a localized swelling applies including how long the lump has been
present, whether it is painful, if it is growing or fluctuating in size and whether it is solitary or
multiple. Findings to look for on examination include:

1. Site
2. Size
3. Definition well defined or ill defined
4. Consistency cystic, solid, soft, hard
5. Surface smooth or irregular
6. Mobility or Fixity to skin or deep tissues
7. Temperature abscess
8. Transilluminable fluid filled
9. Pulsatility
10. Overlying skin changes
11. Local lymphadenopathy

Features suggestive of a benign soft tissue neoplasm include smaller size, fluctuation in size
(malignant tumours dont regress in size), cystic lesions, welldefined lesions, fluid filled lesions
and soft / fatty lesions

Features suggestive of a potential malignant soft tissue neoplasm include larger lesions (>5cm),
rapid growth in size, a solid lesion, an illdefined lesion, an irregular surface, associated
lymphadenopathy and systemic upset (weight loss, loss of apetite, fatigue).

Any lesion where the nature of the swelling is unknown may need imaging by MRI (or
ultrasound to confirm a cystic lesion) or biopsy for histological diagnosis and referral to a
specialist is advised
Benignsofttissuetumours

34

Benign soft tissue tumours can involve any of the nonbony connective tissues, nerves or vessels.
The commonest is a lipoma (a neoplastic proliferation of fat) which usually occurs in the
subcutaneous fat but can occur in muscle. Subcutaneous lipomas can be large and may not be
particularly well defined but their location and consistency points to their diagnosis.

The giant cell tumour of tendon sheath is a small firm swelling usually found on the flexor
tendon sheath of a finger. They may or may not be painful and can erode bone if large enough.
Macroscopically they are pigmented lesion and histologically contain multinucleated giant cells
and haemosiderin. They can be excised but they have a fairly high chance of recurrence. Similar
lesions can occur within a synovial joint (commonly the knee) in a localized or diffuse form amd
can cause pain and effusions. When in a joint the lesion is known as Pigmented Villonodular
Synovitis (PVNS).

Othermusculoskeletalsofttissueswellings

A ganglion cyst occurs around a synovial joint or a synovial tendon sheath. It may form as a
result of herniation or outpouching of a weak portion of joint capsule or tendon sheath. The
weakness can be developmental (eg juvenile Bakers cyst) or as a result of underlying joint
damage / arthritis with buildup of pressure within the joint (adult Bakers cyst, mucous cyst of
DIP joint, wrist ganglion). Ganglion cysts are welldefined, may be quite firm and readily
transilluminate. Excision may be required for localized discomfort or cosmesis.

Bursitis A bursa is a small fluid filled sac lined by synovium around a joint which prevents
friction between tendons, bones, muscle and skin. There are numerous bursae around different
joints and bony prominences. Commonly inflamed bursae which usually occur after repeated
pressure or trauma and which may present as a soft tissue swelling include prepatellar bursitis,
olecranon bursitis and bunions (bursitis over the medial 1st metatarsal head in hallux valgus).
Bacterial infection can cause a bursal abscess (usually from a small wound on the limb) and gout
may cause a bursitis. With inflammatory bursitis the fluid component of the swelling usually
subsides but a thickened bursal sac may be left. Recurrence may occur and excision may be
required but problems can occur with scarring.

Sebaceous cysts and implantation dermoids can occur on a limb and may require excision and/or
biopsy.

Abscesses abscesses on a limb can occur from cellulitis, bursitis, penetrating wound or infected
sebaceous cysts. Abscesses will not resolve with antibiotics alone and require incision and
drainage.

Malignantsofttissuetumours

Malignant soft tissue tumours arising from the connective tissues are known as sarcomas.
Sarcomas are relatively uncommon accounting for less than 1% of all malignant tumours.
Sarcomas can arise from and are named according to the tissue type from which they arise:

Angiosarcoma is a malignant tumour from blood vessels
Fibrosarcoma and Malignant Fibrous Histiocytoma arise from fibrous tissue
Liposarcoma arises from fat.
Rhabdomyosarcoma is a malignant tumour of skeletal muscle.
Synovial sarcoma originates in the synovial lining of joints or tendons.

Sarcomas most commonly present between the ages of 50 and 70 but can occur at any age. Again
if there is doubt over the nature of a soft tissue swelling, referral to a specialist is recommended
with imaging and biopsy as required. Once the diagnosis is established, the cancer is graded and
staged whilst treatment is usually surgical with adjunctive chemotherapy and/or radiotherapy.
Surgery usually involves radical or wide local excision with limb salvage surgery or amputation if
a functional limb cannot be maintained.

35

36

ElectiveSurgery

Elective (scheduled) orthopaedic surgery involves the treatment of nonemergency or cold
musculoskeletal conditions.

Often patients are referred for the assessment of a musculoskeletal disorder and in many cases
nonoperative or conservative management is decided as the most appropriate treatment
option. Conservative treatments may include lifestyle advice, rest, physiotherapy, orthoses,
mobility, aids, splints, injections and medical treatments. Onward referral to rheumatology,
podiatry, physiotherapy, neurology, orthotics, occupational therapy, interventional radiology or
an appropriate orthopaedic subspecialty may be appropriate.

In general terms, surgical management should only be considered when there is an appropriate
surgical solution to a problem and when conservative measures have not controlled the patients
symptoms or if surgical intervention is more appropriate (eg tumour surgery). The decision to
undertake surgery is based on the underlying condition, the prognosis without surgical
intervention, the degree of symptoms which the patient is experiencing, the disability caused by
the condition and the status of the patients health. Operative intervention should only be
considered after thorough consultation involving appropriate consenting, explanation of the
risks and benefits of the procedure and explanation of the alternatives to surgery.

Common orthopaedic elective surgical procedures involve the surgical management of:

1. Arthritis
2. Soft tissue inflammatory problems eg tendonitis, tendon rupture
3. Correction of deformity
4. Nerve decompression
5. Joint instability
6. Joint contractures
7. Chronic infection
8. Tumour diagnosis and treatment

Some elective cases are obviously more urgent than others (suspected cancer).

Surgicalstrategiesforthemanagementofanarthriticjoint

Several strategies exist for the surgical management of an arthritic joint:
Arthroplasty/JointReplacement

Arthroplasty literally means the reshaping of a joint. In general terms this is synonymous with
joint replacement although it can be used to describe the removal of a diseased joint excision or
resection arthroplasty.

Joint replacement involves either replacement of part of the joint (replacing one half of the joint
is known as hemiarthroplasty) or the whole joint (known as total joint replacement). The most
successful joint replacements are hip and knee replacements which usually provide good
function, staisfactory pain relief and last a reasonable length of time. Complication rates are low.
Other established joint replacements exist for the shoulder (glenohumeral joint), elbow, ankle, 1st
MTP joint of the great toe, MCP joints of the hand and wrist.

37


Figure 13: The components of total hip replacement. Source: Smith E ().

Joint replacements can be made of stainless steel, cobalt chrome, titanium alloy, polyethylene and
ceramic. Components may or may not be cemented with advantages and disadvantages of both.
The surfaces can consist of a metalpolyethylene, ceramicpolyethylene, ceramicceramic or
metalmetal bearing couple. There is no single ideal material or combination of materials for a
joint replacement and ultimately the joint replacement will fail due to loosening (caused by wear
particles producing an inflammatory response or high stresses) or breakage of the joint
replacement components. Metal particles can cause an inflammatory granuloma (known as a
pseudotumour) which can cause muscle and bone necrosis, polyethylene particles can cause an
inflammatory response in bone with subsequent bone resorption (known as osteolysis) resulting
in loosening and ceramics can shatter with fatigue due to their brittleness.

Once a joint replacement fails a revision (redo) procedure to remove the old components and
insert a new replacement is much more difficult than the first procedure, the complication rates
are higher, functional outcomes are usually poorer and patient satisfaction is less. In general
terms, the younger the patient, the higher the demands on the joint replacement will be and the
higher the likelihood is of early failure of the joint replacement and revision surgery.

Serious complications of joint replacement can occur including deep infection, recurrent
dislocation, neurovascular injury, pulmonary embolism and medical complications (renal failure,
MI, chest infections etc).

Deep infection can cause a serious problem which is why in orthopaedics in particular, strict
aseptic and antiseptic precautions are taken in theatre. If a fulminant infection is diagnosed early
(within the first 23 weeks) surgical washout & debridement and prolonged parenteral antibiotic
therapy (around 6 weeks) can be attempted to salvage the artificial joint. This strategy is around
50% successful. Deep infections present for longer than 3 weeks or so tend not to be salvageable
by washout as the infecting bacteria adhere to the foreign surfaces and form a Biofilm which
prevents the patients immune system attacking. In this situation, removal of the infected
implants and all foreign material (including cement) which requires extensive surgery is usually
required. The patient is usually left without a joint for around 6 weeks and given parenteral
antibiotics. Once the infection is under control (wound healed, clean and dry, CRP reduced) a
revision (redo) joint replacement is performed with more complex joint replacement
components. This strategy is around 8090% successful in eradicating infection however
throughout this process the soft tissues scar and lose elasticity. The joint inevitably stiffens and
the overall functional outcome is usually compromised.

Early and late complications of joint replacement are listed below:

Early local complications:

38

Infection, dislocation, instability, fracture, leg length discrepancy, nerve injury, bleeding,
arterial injury / ischaemia, bleeding, DVT

Early general complications:

Hypovolaemia, shock, acute renal failure, MI, ARDS, PE, chest infection, urine infection.
There is approximately a 0.2% chance of dying as a result of a hip or knee replacement.

Late local complications:

Infection (from haematogenous spread), loosening, fracture, implant breakage,
pseudotumour formation

Excisionorresectionarthroplasty

This involves the removal of bone and cartilage of one or both sides of a joint. Whilst this may be
quite disabling for larger joints (this was the first surgical procedure for hip OA), it can be an
effective procedure for smaller joints (eg first carpometacarpal joint in hand, Kellers procedure
for Hallux Valgus). It is also occasionally utilized after failure of hip or shoulder replacement.

Arthrodesis

This means a surgical stiffening or fusion of a joint in a position of function. The remaining
hyaline cartilage of the joint and subchondral bone is removed and the joint is stabilized
resulting in bony union (like fracture healing) and fusion. Whilst this may be good at alleviating
pain, function may be limited particularly in large joints and may increase pressure in
surrounding joints leading to arthritic change. Arthrodesis is good for end stage ankle arthritis,
wrist arthritis and arthritis of the first MTP joint of the foot (hallux rigidus).

Osteotomy

Osteotomy is surgical realignment of a bone which can be used for deformity correction or to
redistribute load across an arthritic joint. In the treatment of arthritis, the aim is to offload the
diseased part of the joint and shift load to an undiseased part (eg from the medial compartment
of the knee to the lateral compartment). Osteotomy can be used for early arthritis in the knee and
hip.

39


Figure 14: (High tibial closingwedge) osteotomy to correct varus deformity.

Softtissueproblems

These include tendonopathies (including tears and ruptures), enthesopathies (inflammation of a
tendinous origin from or insertion into bone), cartilage tears, labrum tears, inflammatory
bursitis, tenosynovitis, capsulitis and noninfective fasciitis. These may be related to
degenerative processes, injuries, overuse, inflammatory conditions (rheumatoid), drugs (eg
quinolone antibiotics, steroids) or chronic disease (renal failure). Many are idiopathic.

Figure 15: Olecranon bursitis. Source: Douglas G et al. (2009).

The vast majority of soft tissue inflammatory problems settle with rest, analgesia and anti
inflammatory medications if appropriate. Some tendons and entheses are amenable to injection
of steroid around the tendon (eg rotator cuff, tennis albow) whilst in others there is substantial
risk of tendon rupture and injection is not advised (Achilles, extensor mechanism of knee).

40

Refractory cases may benefit from surgical debridement (removal of diseased tissue) or
decompression (making more space eg supraspinatus tendonitis & subacromial decompression).
Synovectomy can be performed for the extensor tendons of the wrist in rheumatoid arthritis or
for inflammation of the tibialis posterior tendon to prevent rupture.

Major tendon tears may require splintage (eg Achilles), surgical repair (eg quadriceps or patellar
tendon, occasionally Achilles tendon) or tendon transfer (eg tibialis posterior, extensor pollicis
longus).

Cartilage (meniscal) tears in the knee can be treated with arthroscopic removal (or occasionally
repair) if the pain fails to settle or if the cause mechanical symptoms (locking or catching) and
similarly labral tears of the acetabulum of glenoid can be resected or repaired.

Surgeryforjointinstability

Instability is abnormal motion of a joint (rotation or translation) resulting in subluxation or
dislocation with pain and/or giving way. Common examples include instability from knee
ligament injuries, recurrent subluxation or dislocation of the shoulder, recurrent subluxation or
dislocation of the patella, ankle instability with frequent giving way and spinal instability.

Instability can be a consequence of an injury or can be related to ligamentous laxity. It can also be
predisposed by anatomic variation (eg shallow trochlea of distal femur, femoral neck anteversion
and genu valgum in patellofemoral instability) and can be due to an underlying disease process
(eg cervical spine instability in rheumatoid arthritis, knee hyperextension in polio).

Most cases of joint instability can be managed with physiotherapy to strengthen up surrounding
muscles and to improve proprioception (eg ACL rupture, ankle & shoulder instability) and
splints, calipers or braces may provide additional support.

Surgical strategies for instability consist of soft tissue procedures and bony procedures. Soft
tissue procedures include ligament tightening/advancement (eg ankle instability), ligament
reconstruction using tendon graft (eg ACL reconstruction) or soft tissue reattachment (eg
shoulder instability). In cases of significant ligamentous laxity (eg EhlersDanlos), soft tissue
procedures are highly unlikely to work and a bony procedure may be required (eg fusion). In
cases where there is a skeletal predisposition to dislocation (eg patellar instability) an osteotomy
may improve joint stability. Spinal instability may cause pain, nerve root compression or spinal
cord compression and may require fusion of the abnormal spinal motion segment.

Correctionofdeformity

Correction of deformity may be required to improve function, to prevent arthritis or to improve
cosmesis. Deformities may be congenital (eg limb malformation), developmental (eg bow legs),
acquired (posttraumatic), or idiopathic (hallux valgus, claw toes).

Congenital malformations may require complex bony and soft tissue surgery to restore as much
function as possible and some are best served by functional amputation.

Angular deformity of the long bones of the lower limb may result in early arthritis of the knee or
ankle due to abnormal distribution of force. Correction can be achieved by growth plate
manipulation surgery or by osteotomy.

Leg length discrepancies can be corrected by either shortening the longer limb or lengthening the
short limb using a special external fixator (known as the Ilizarov technique).

Foot deformities can give rise to pressure problems with footwear. Osteotomy, arthrodesis, soft
tissue procedures and joint excisions may help.

41

Spine deformities can be performed for cosmesis or to improve wheelchair sitting. Severe
scoiliosis can also result in a restrictive respiratory defect and correction may be performed to
prevent this.

Nervedecompression

Peripheral nerves can be trapped at various sites in the upper and lower limbs with the most
common sites being the median nerve at the wrist (carpal tunnel syndrome) and the ulnar nerve
at the elbow (cubital tunnel syndrome). Symptoms can be improved by nerve decompression
surgery.

Spinal nerve roots can be compressed by disc material or bony osteophytes causing a
radiculopathy which may require spinal decompression or discectomy.

Jointcontractures

Joint contractures may occur due to neuromuscular disease, spasticity (eg stroke), soft tissue
imbalance, arthritis, injury, fibrosing disease (Dupuytrens), disuse or burns. Contractures may
be passively correctable and may be amenable to splintage, physiotherapy and medications
(Baclofen, Botox injections) to relieve spasticity. Fixed or resistant contractures may require
surgical treatment which may consist of tendon lengthening, tendon transfer, release or
lengthening of tight soft tissues or bony procedures (osteotomy, arthrodesis).

Infection

Infections often present acutely to the orthopaedic department and soft tissue abscesses may
require surgical incision and drainage. The treatment of Osteomyelitis has been previously
discussed. Septic arthritis can result in early arthritis of a joint with the principles of surgical
management of an arthritic joint outlined above. If preforming a joint replacement, one must be
sure that no ongoing or active infection is present.

Tumours

As detailed previously orthopaedics may be involved in the diagnosis of and surgical treatment of
soft tissue and skeletal tumours.

42

PaediatricOrthopaedics

As mentioned in the introduction of this guide, orthopaedics has its historical roots in the
treatment of skeletal deformities of children.

An understanding of normal musculoskeletal development of children is essential to know what
is normal and what is abnormal/pathological. Frequently normally developing children are
referred to paediatrics or childrens orthopaedics with parental concerns about the appearance,
function or development of their limbs.

Normaldevelopmentalmilestones

To determine what might be considered delayed or abnormal development, particularly in the
diagnosis of developmental delay or neuromuscular disease one needs to know the approximate
timescales of normal musculoskeletal development:

Sits alone, crawls 69 months
Stands 812 months
Walks 1417 months
Jumps 24 months
Manages stairs independently Age 3

In addition, landmarks of neurological development include:

Loss of primitive reflexes (Moro reflex, stepping reflex, rooting, grasp reflex, fencing
posture etc) by 16 months.
Head control 2 months
Speaking a few words 912 months
Eats with fingers, uses spoon 14 months
Stacks four blocks 18 months
Understands 200 words, learns around 10 words/day 1820 months
Potty trained 23 years

Note that there can be considerable variation between children including siblings and the first
child in a group to sit may be the last to walk.

43


Figure 16: Chronologic progression of gross motor development during the rst 12 month. Refer
to Child Health block for more information on developmental milestones. Source: Gerber JR et al.
(2010)

Normallowerlimbdevelopmentandcommonvariations
Disordersofkneealignment

Children at birth normally have varus knees (bow legs) which become neutrally aligned at
around 14 months, progressing to 10 to 15 valgus (knock knees) at age 3 and then gradually
regress to the physiologic valgus of 6 by around the age of 79. Parents may often be concerned
at the appearance however the vast majority develop normal alignment and most cases need
reassurance only. Some people develop minor degrees of varus or valgus alignment which often
can be familial.

Considerable variation exists and the normal range varies by around. Pathological varus or
valgus is where alignment is considered outside the normal range (+/ 6 from mean value for
age). Measurements can be taken on xrays and charted against normal reference ranges.

A valgus deformity at the knee will result in a more of a knock knee appearance with a larger gap
than normal between the feet/ankles. A varus deformity will result in a larger gap between the
knees. The majority of cases of bow legs or knock knees will resolve by the age of 10 but genu varum
or excessive genu valgum after the age of 10 may require surgery. Many cases are idiopathic, whilst
some are familial. Some cases may be due to an underlying skeletal disorder (skeletal dysplasia,
Blounts disease), physeal injury with growth arrest (usually unilateral) or biochemical disorder
(rickets).
GenuVarum(Bowlegs)

Excessive genu varum may be due to a growth disorder of the medial proximal tibial physis
known as Blounts disease resulting in marked and persisting (beyond 45 years) varus
deformity. This may require surgical correction by osteotomy. The condition can also occur in
adolescence where growth plate restriction on the medial side with a small plate and screws may
be required. Other rarer causes of pathologic genu varum include rickets, tumour
(osteochondroma), traumatic physeal injury and skeletal dysplasia. Persistent bow legs are at
risk of early onset medial compartment osteoarthritis.

44

GenuValgum(knockknees)

Causes of pathologic genu valgum include rickets, tumours (enchondromatosis), trauma and
neurofibromatosis whilst some cases are idiopathic. Again excessive deformities can be corrected
by osteotomy or growth plate manipulation surgery.

Figure 17: Two types of knee deformities. Source: Fauci A et al. ().

Intoeing

Intoeing refers to a child who, when walking and standing will have feet that point toward the
midline. The abnormality is often exaggerated when running and children are felt by their
parents to be clumsy and wear through shoes at an alarming rate. There are a number of causes
of intoeing

Femoral neck anteversion as part of normal anatomy the femoral neck is slightly anteverted
(pointing forwards). Excess femoral neck anteversion can give the appearance of intoeing (as
well as knock knees). However the degree of apparent intoeing is not of a magnitude which
would warrant surgical intervention.

Internal tibial torsion the bone can be rotated inward about its vertical axis but as this is a
normal variation, it should ignored.

Forefoot adduction can cause the apparent intoeing. There remains debate about whether
surgery is useful in cases which persist after 7 or 8 years of age. Certainly surgery should not be
considered before this age as the majority resolve in time.
Flatfeet

Flat feet are part of normal variation and usually do not reflect underlying pathology. At birth all
feet are flat, as we begin to walk and the muscles develop the arch will also develop. Some
children continue to have flat feet which persist into adulthood without any functional problem.

The key is to determine if the flat feet are mobile or fixed. Mobile/flexible flat feet are those
where the flattened medial arch forms with dorsiflexion of the great toe (Jack test). Flexible flat
footedness may be related to ligamentous laxity, may be familial or may be idiopathic. The flat
footedness may only be dynamic (present on weight bearing only). Flexible flatfootedness in
children is a normal variant. Medial arch support orthoses are not required. (In adults mobile flat
foot may be related to tibialis posterior tendon dysfunction see later).

In the rigid type of flat footedness the arch remains flat regardless of load or great toe
dorsiflexion. This implies there is an underlying bony abnormality (tarsal coalition where the
bones of the hindfoot have an abnormal bony or cartilaginous connection) which may require
surgery. It also may represent an underlying inflammatory disorder or a neurological disorder.

45


Curlytoes

Minor overlapping of the toes and curling of toes is common with the fifth toe is most frequently
affected. Again most will correct without intervention but they can occasionally cause discomfort
in shoes and persistent cases in adolescence may require surgical correction.

Paediatrichipproblems
DevelopmentalDysplasiaoftheHip(DDH)

DDH involves dislocation or subluxation of the femoral head during the perinatal period which
affects the subsequent development of the hip joint. It affects up to 5 in 1000 babies and girls are
more commonly affected than boys accounting for 80% of cases. It is more common in the left hip
(due to intrauterine position?) but in 20% of cases is bilateral. Risk factors include positive
family history of DDH, breech presentation, first born babies, Downs syndrome and the presence
of other congenital disorders (talipes, arthrogryposis).

If left untreated the acetabulum is very shallow and in more severe cases a false acetabulum
occurs proximal to the original one with a shortnened lower limb. Severe arthritis due to reduced
contact area can occur at a young age and gait / mobility may be severely affected.

All hips should be examined clinically shortly after birth. Signs of DDH include shortening,
asymmetric groin/thigh skin creases and a click or clunk on the Ortolani or Barlow manoeuvres.
Unstable hips with a positive Ortolani test (reducing a dislocated hip with abduction and anterior
displacement) or Barlow test (dislocatable hip with flexion and posterior displacement) require
further evaluation with ultrasound which should detect a dislocated hip, an unstable hip or a
shallow acetabulum. Xrays cannot be used for the early diagnosis of DDH as the femoral head
epiphysis is unossified until around 46 months but xrays are the investigation of choice after
this age.

Figure 18: Ortolani (left) and Barlow test (right). Source: French LM and Dietz FR (1999).


Early diagnosis is key to the success rates of treatment. Mild cases with a slightly shallow
acetabulum and mildly dislocatable but reduced (in joint) hip can be closely observed with serial
examination and ultrasound to ensure the hip remains reduced. Dislocated or persistently
unstable hips are reduced and held with a special harness known as a Pavlik harness which

46

keeps the hips in comfortable flexion and abduction thus maintaining reduction (overflexing and
abducting the hip can result in avascular necrosis). The Pavlik harness is used fulltime for
around 6 weeks and parttime for a further 6 weeks once the hip is confirmed to be stable. A
Pavlik harness can be used up to around 46 months of age and the success rate is 8595%.

For children with persistent dislocation or who are diagnosed later than 46 months and up to
around 18 months (walking age) the hip may be able to be reduced by closed manipulation under
anaesthetic with an arthrogram (injection into the joint and fluoroscopy) to confirm concentric
reduction. However there may be soft tissues preventing reduction which may require open
reduction with surgery to clear obstructing soft tissues. After open or closed reduction the child
is placed in a hip spica cast with a cross bar incorporated to hold the hips abducted for around 3
months followed by a splint which permits some movement for a further few months.

For children with persistent dislocation over 18 months old open reduction is much more likely
to be required and the acetabulum is likely to be very shallow by this stage. Typically the child
will need an open reduction to clear soft tissues and may also need an osteotomy to shorten and
rotate the femur and/or pelvic osteotomy to deepen and reorientate the acetabulum. Persistent
or undiagnosed DDH at this stage tends to have a poorer prognosis.
Transientsynovitisofthehip

Transient synovitis is as its name suggests a selflimiting inflammation of the synovium of a joint,
most commonly the hip. It commonly occurs shortly after an upper respiratory tract infection
(usually viral) although sometimes no cause is found. Typical age is between 2 and 10 and boys
are more commonly affected than girls.

Transient synovitis is the commonest cause of hip pain in childhood although other pathologies
including septic arthritis, Perthes disease and Juvenile Idiopathic Arthritis or Rheumatoid
arthritis must to be excluded. Presentation is with limp or reluctance to weight bear on the
affected side. Range of motion may be restricted (but not as much pain or loss of motion as septic
arthritis). The child may have a low grade fever but is not systemically unwell or septic.

Radiographs can exclude Perthes disease whilst a normal or near normal CRP and a clinical
picture more suggestive of transient synovitis may exclude septic arthritis. If there is any doubt
aspiration of the hip under anaesthetic or open surgical drainage may be performed to limit
cartilage damage from potential bacterial infection. MRI may also be useful in equivocal cases as
osteomyelitis of the proximal femur is a further possible diagnosis.

Once a more serious casuse of hip pain is excluded, treatment is with a short course of NSAIDs
and rest. Pain generally resolves within a few weeks but if there is no resolution then another
cause for hip pain (JIA, early Perthes) should be sought.
Perthes

Perthes disease (aka LeggCalvePerthes disease) is an idiopathic osteochondritis of the femoral
head which usually occurs between the ages of 4 to 9 and is more common in boys (around 5:1),
particularly very active boys of short stature. The femoral head transiently loses its blood supply
resulting in necrosis with subsequent abnormal growth. The femoral head may collapse of
fracture. Subsequent remodeling occurs however the shape of the femoral head and congruence
of the joint is determined by age of onset (with older children faring worse) and the amount of
collapse. In incongruent joint will lead to early onset of arthritis and severe cases may require hip
replacement in adolescence or early adulthood.

Affected children present with pain and a limp. Most cases are unilateral and bilateral cases may
represent an underlying skeletal dysplasia or a thrombophilia. Loss of internal rotation is usually
the first clinical sign followed by loss of abduction and later on a positive Trendellenburg test
from gluteal weakness.

47


Figure 19: Positive Trendelenburg test on the right side, where the hip drop to the left side.
Source: Dandy D and Edwards DJ (2009).

There is no specific treatment other than regular xray observation and avoidance of physical
activity. Approximately 50% of cases do well. In some cases the femoral head becomes
aspherical, flattened and widened. The lever arm of the abductor muscles is altered resulting in
weakness (Trendellenburg positive). Occasionally the femoral head may sublux (partially
dislocate) requiring an osteotomy of the femur or acetabulum.
SUFESlippedUpperFemoralEpiphysis

Slipped Upper Femoral Epiphysis is a condition mainly affecting overweight prepubertal
adolescent boys where the femoral head epiphysis slips inferiorly in relation to the femoral neck.
Girls are less commonly affected and hypothyroidism or renal disease may predispose to SUFE.

In the condition, the growth plate (physis) is not strong enough to support body weight and the
femoral epiphysis slips due to the strain. A growth spurt may preclude the onset and puberty
may be delayed (idiopathic or hypothyroidism). 1/3 of cases are bilateral.

Cases can be acute (sudden onset), chronic or acuteonchronic. Patients have pain and a limp.
The pain may be felt in the groin (like other hip pathology) however the major pitfall is that
patients can present purely with pain in the knee (due to the obturator nerve supplying both
the hip and knee joint) and the diagnosis can be missed as an unwary clinician may fail to
examine the hip, concentrating solely on the knee and treat as a benign knee condition. Loss of
internal rotation of the hip is the predominant clinical sign. Xray changes may be subtle and
a lateral view must be obtained to detect mild degrees of slip.

The treatment of SUFE is urgent surgery to pin the femoral head to prevent further slippage. The
greater the degree of slip the worse the prognosis and some cases may require hip replacement
in adolescence or early adulthood. The prognosis for mild slips is usually favourable. For severe
acute slips gentle manipulation may be attempted but this risks avascular necrosis. Chronic
severe slips may require an osteotomy.

Paediatric&Adolescentkneeproblems

48

Remember to examine the hip to ensure no serious hip disorder is missed.

Extensormechanismproblems

Knee extensor mechanism pain is a fairly common occurrence during adolescence as body weight
increases and sporting activities increase. Patellar tendonitis (jumpers knee) can occur which is
selflimiting and requires rest and possibly physiotherapy.

Apophysitis (inflammation of a growing tubercle where a tendon attaches) can occur at either
end of the patellar tendon due to repetitive strain. Inflammation of the tibial tubercle apophysis
is more common and is known as OsgoodSchlatters disease. Inflammation of the inferior pole of
patella is known a SindingLarsenJohanssen disease. Again these are selflimiting conditions
requiring rest +/ physiotherapy. Patients may be left with a bony prominence which does not
require surgery.

Figure 20: Difference of OsgoodSchlatters disease and SindingLarsenJohanssons disease.
Source: Miller MD (2012).
Adolescentkneepain

Anterior knee pain (patellofemoral dysfunction) is common in adolescence, especially in girls.
The aetiology is unclear and may be due to muscle imbalance, ligamentous laxity and subtle
skeletal predisposition (genu valgum, wide hips, femoral neck anteversion). There may be
softening of the hyaline cartilage of the patella (chondromalacia patellae).

The majority of cases are selflimiting and the mainstay of treatment is physiotherapy to
rebalance the muscles. Most patients grow out of the condition. Occasionally resistant cases
may require surgery to shift the forces on the patella (known as a tibial tubercle transfer)
however the results can be unpredictable.
Patellarinstability

Dislocation and subluxation of the patella is most common in adolescence and may be related to
trauma with a tear in the medial patellofemoral ligament and may be predisposed to by
ligamentous laxity and varitions in bony anatomy (shallow femoral trochlea, valgus, hip
anteversion).

Dislocations may cause osteochondral fracture with a fragment of hyaline cartilage with or
without subchondral bone breaking off. Small fragments may need retrieved by arthroscopic
surgery whilst larger fargments may be fixed.

49

20% of first time dislocations go on to have a second episode of dislocation and 10% have
multiple dislocations. Many patients stabilize as they grow older and physiotherapy may help.
Recurrent dislocation may require surgery to correct any bony predisposition or to reconstruct
the medial patellofemoral ligament.
Osteochondritisdissecans(OCD)

OCD as previously discussed is an osteochondritis where a fragment of hyaline cartilage with
variable amount of bone fragments and breaks off the surface of the joint. The knee is the most
common joint affected with the medial femoral condyle the most common site. The condition
usually occurs in adolescence but can occur later in adulthood. Patients present with poorly
localized pain, effusion and occasionally locking. Defects can be difficult to see on standard xrays
and may require special views or MRI to diagnose. A quarter of cases are bilateral.

OCD can result in loose bodies within the knee joint and a pothole on the surface which
predisposes to osteoarthritis. Lesions which are at risk of breaking off (with fluid signal behind
them on MRI) may be fixed and loose fragments may require removal.
Meniscalproblems

Meniscal tears can occur in children and adolescents with a higher proportion of peripheral or
bucket handle meniscal tears which may benefit from meniscal repair. Moreover young patients
have a higher chance of healing with a meniscal repair.

Some children have an abnormally shaped discoid meniscus (usually the lateral meniscus) which
is circular rather than Cshaped and can be a source of pain and a popping sensation.
Arthroscopic partial menisectomy may help.

Paediatricfoot&ankleproblems
TalipesEquinovarus(Clubfoot)

Talipes equinovarus is a congenital deformity of the foot affecting 1 in 800 births and is due to in
utero abnormal alignment of the joints between the talus, calcaneus and navicular. Around 50%
of cases are bilateral. The abnormal alignment of these joints results in contractures of the soft
tissues (ligaments, capsule & tendons) resulting in a deformity consisting of ankle equinus
(plantarflexion), supination of the forefoot and varus alignment of the forefoot which are not
immediately correctable. Boys are twice as commonly affected than girls, there may be a genetic
link with a positive family history and it is more common in breech presentation.
Oligohydramnios (low amniotic fluid content) is another risk factor and it is occasionally part of
another skeletal dysplasia.

Figure 21: Newborn with clubfoot on the right and normal foot on the left. Source: Bass A (2012).

50


Again the condition is eminently treatable with early splintage and diagnosis is usually obvious
however delayed presentations (uncommon in modern healthcare systems) can result in fixed
deformity with the child walking on the outside of their foot. Late deformity is very difficult to
correct and requires extensive surgery (soft tissue +/ bony procedures) with less satisfactory
results. Surgery may also be required for cases resistant to splintage.

The technique of splintage, known as the Ponseti technique, is commenced as soon as possible
after birth and the deformities are corrected progressively in stages and held in plaster casts
with 5 or 6 weekly cast changes. 80% of children require a tenotomy of the Achilles tendon (a
minor procedure) to maintain full correction. Once full correction is achieved the child is then
placed in a brace consisting of boots attached to a bar which is worn 23 hours a day for 3 months
and used during sleep until the age of 3 to 4 to try to prevent recurrence.

Figure 22: First holding cast with Ponseti method. Source: Bass A (2012).

Tarsalcoalition

This is a condition where there is an abnormal bridge (bony, fibrous or cartilaginous) between
the calcaneus and navicular or between the talus and calcaneus. It can lead to a painful fixed flat
foot deformity in older children. Symptoms may improve with splintage / orthotics whilst
resistant pain may require surgery to remove the abnormal connection.
Halluxvalgus

Hallux valgus can occur in late adolescence and usually has a strong family history. Surgical
correction in this age group carries a risk of recurrence of the deformity later in life.

Paediatric/Adolescentspineproblems

Remember back pain in a child or adolescence is a red flag sign have a low threshold for
referral/investigation. Infections (discitis) and tumours (eg osteoid osteoma) can occur in
children and spondylolisthesis (see below) may require prompt surgical treatment.
Scoliosis

Scoliosis is a lateral curvature of the spine (and also rotational deformity) which can be
idiopathic (most common) or secondary to neuromuscular disease, tumour (eg osteoid osteoma),
skeletal dysplasia or infection. Idiopathic scoliosis is more common in females and presents in
adolescence with concerns regarding cosmetic appearance. Younger children with scoliosis
usually have an underlying cause and may progress more readily to a severe curve. Any painful
scoliosis warrants urgent investigation (MRI for tumour or infection).

Mild, nonprogressive scoliosis (majority of cases) does not require surgery. Larger curves may
require surgery for cosmesis or to improve wheelchair posture (neuromuscular disease). Severe

51

curves can result in a restrictive lung defect and surgery may be required to prevent breathing
difficulties.

Surgery is complex and requires vertebral fusions and long rods connecting the posterior
elements of the spine. Correction of larger curves carries a risk of spinal cord injury
(intraoperative monitoring may be used).

Spondylolisthesis

This is slippage of one vertebra over another and usually occurs at the L4/L5 or L5/S1 level. It
can be due to a developmental defect or a recurrent stress fracture of the posterior elements
which fails to heal.

Spondylolisthesis usually presents in adolescence. Increased body weight and increased sporting
activity have been implicated. Patients present with low back pain and may have a radiculopathy
with severe slippage. They may have a paradoxical flat back due to muscle spasm and can
present acutely with a characteristic waddling gait.

Minor degrees of slippage may be observed and treated with rest & physiotherapy. More severe
slips may require stabilization and possibly reduction (however this risks neurological injury).

52

AdultRegionalOrthopaedics
LumbarSpine

Many people experience back pain at some point during their life and back pain is one of the
most common reasons for ill health resulting in time off work. The vast majority of cases will be
mechanical back pain with no serious underlying pathology. Many cases will be as the result of
awkward twisting or poor lifting technique leading to acute muscular or ligamentous sprains or
strains. Back pain may also be related to obesity, lack of physical activity or early osteoarthritis
(known as spondylosis). Advice and analgesia, with or without physiotherapy, is often enough to
treat the acute episodes and prevent further injury. However occasional cases of back pain may
have serious underlying pathology and it is crucial to recognize red flags from history and
examination which warrant further investigation.
MechanicalBackPain

This can be thought of as recurrent relapsing and remitting back pain with no neurological
symptoms. The pain is worse with movement (mechanical) and relieved by rest. Patients tend to
be between the age of 20 and 60 and have had several previous flareups. No red flags are
present.

Causes implicated include obesity, poor posture, poor lifting technique, lack of physical activity,
depression, degenerative disc prolapse, facet joint OA and spondylosis. Spondylosis is where the
intervertebral discs lose water content with age resulting in less cushioning and increased
pressure on the facet joints leading to secondary OA.

Treatment involves analgesia and physiotherapy. Patients should be reassured that they do not
have a serious problem and should be urged to maintain normal function and return to work
early. Bed rest is not advised as this will lead to stiffness and spasm of the back which may
exacerbated disability.

If a single level (2 adjacent vertebrae) is affected by OA or instability (excessive motion caused by
a degenerate disc) is diagnosed (typically on MRI) and if the patient has not improved despite
physio and conservative management and if there are no other adverse secondary gain or
behavioural issues which adversely affect outcome of surgery (disability allowance appeal,
compensation claim, psychological dysfunction) then some patients may benefit from spinal
stabilization surgery. However this is the vast minority of patients as most have multilevel
disease of the spine for which there is no role for surgery. Furthermore long term results of
spinal stabilization suggest recurrence of symptoms and no benefit after around 5 years from
surgery and spinal surgery for back pain remains controversial.
Acutedisctear/Discogenicbackpain

An acute tear can occur in the outer annulus fibrosis of an intervertebral disc which classically
happens after lifting a heavy object (eg lawnmower). The periphery of the disc is richly
innervated and pain can be severe. Pain is characteristically worse on coughing (which increases
disc pressure). Symptoms usually resolve but can take 23 months to settle. Analgesia and
physiotherapy are the mainstay of treatment.
Sciatica/LumbarRadiculopathy

If a disc tear occurs, the gelatinous nucleus pulposis can herniate or prolapse through the
tear. Disc material can press (impinge) on an exiting nerve root resulting in pain and altered
sensation in a dermatomal distribution as well as reduced power in a myotomal distribution.
Reflexes (a test of sensory and motor function may also be reduced. (Note these are lower motor
neurone signs).

53

The commonest site for this to occur in the spine is the lower lumbar spine with the L4, L5 and
S1 nerve roots contributing to the sciatic nerve and pain radiating to the part of the sensory
distribution of the sciatic nerve (hence the term sciatica). The radicular pain is felt as a
neuralgic burning or severe tingling pain, often like severe toothache radiating down the back of
the thigh to below the knee. (Note back pain can radiate to the buttock and thigh but not below
the knee). Patients usually have a positive sciatic stretch test and also may have a crossover sign
where sciatic stretch testing of the opposite side

Usually in the lumbar spine, the nerve root corresponding to the lower of the two vertebra in the
affected segment is compressed and the following typical patterns occur:

L3/4 prolapse L4 root entrapment pain down to medial ankle (L4), loss of quadriceps
power, reduced knee jerk

L4/5 prolapse L5 root entrapment pain down dorsum of foot, reduced power Extensor
Hallucis Longus and tibialis anterior

L5/S1 prolapse S1 root entrapment pain to sole of foot, reduced power planarflexion,
reduced ankle jerks

However dermatomal and particularly myotomal distributions can vary and the nerve root
affected isnt always entirely accurate (may localize to one side and two adjacent nerve roots).
Furthermore a very lateral disc prolapse can cause impingement of the nerve root corresponding
to the vertebra above (eg L4/5 L4 nerve radiculopathy).

Figure 23: At the L45 junction: a laterally placed prolapse may compress the L4 root (A); a more
central prolapse will compress L5 (B); a central prolapse will lead to cauda equina (C) and
formation of osteophytes in the lateral canal will also lead to root compression. Source: Dandy D
and Edwards DJ (2009).

54

First line treatment is with analgesia, maintaining mobility and physiotherapy. Occasionally
drugs for neuropathic pain (eg Gabapentin) can be used if leg pain is particularly severe. The
majority of cases are dealt with in primary care with around 8090% of disc prolapses recovering
spontaneously by 3 months. Very occasionally surgery (discectomy) is indicated when pain is not
resolving despite physiotherapy and there are localising signs suggesting a specific nerve root
involvement and positive MRI evidence of nerve root compression. Again evidence of secondary
gain (compensation claim, disability benefit) or psychological dysfunction is usually a predictor
of poor outcome of surgery and a contraindication. Discectomy has a small risk of permanent
neurologic injury (less than 1%).
Bonyrootentrapment

OA of the facet joints can result in osteophytes impinging on exiting nerve roots. Surgical
decompression may be performed in suitable candidates.
Spinalstenosisandspinalclaudication

With spondylosis, the combination of bulging discs, bulging ligamentum flavum and
osteophytosis, the cauda equina of the lumbar spine has less space known as spinal stenosis
and multiple nerve roots can be compressed / irritated.

Sufferers tend to over 60 and characteristically have claudication (pain in the legs on walking).
However, in contrast to vascular claudication (from PVD), the claudication distance is inconsistent,
the pain is burning (rather than cramping), pain is less walking uphill (spine flexion creates more
space for the cauda equina) and pedal pulses are preserved.

Again if symptoms fail to improve with conservative management and there is MRI evidence of
stenosis, surgery may be performed (decompression) to help alleviate symptoms.
Osteoporoticcrushfractures

With severe osteoporosis, spontaneous crush fractures of the vertebral body can occur leading to
acute pain and kyphosis. A minority of patients go on to have chronic pain due to altered spinal
mechanics. Treatment is usually conservative however some clinicians including interventional
radiologists have tried balloon vertebroplasty (involves inserting a balloon into the vertebral
body under fluoroscopic guidance, inflating a balloon and injecting cement to fill the void) for
patients with chronic pain with some good results obtained. The long term results have not been
fully evaluated and there is a small risk of neurological injury.
Caudaequinasyndrome

Occasionally a very large central disc prolapse can compress all the nerve roots of the cauda
equina producing a clinical picture known as cauda equina syndrome. This is a surgical
emergency as affected nerve roots include the sacral nerve roots (mainly S4 & S5 but variable
and others contribute) controlling defaecation and urination. Prolonged compression can
potentially cause permanent nerve damage requiring colostomy and urinary diversion and
urgent discectomy way prevent this catastrophe. Symptoms and signs of cauda equina syndrome
are one of the red flags of the spine which signify serious underlying pathology requiring
urgent management.

Patients usually have bilateral leg pain, paraesthesiae or numbness and complain of saddle
anaesthesia numbness around the sitting area and perineum. Altered urinary function is
typically urinary retention but incontinence can also occur. Faecal incontinence and constipation
can also occur. In essence any patient with bilateral leg symptoms/signs with any suggestion of
altered bladder or bowel function is a cauda equina syndrome until proven otherwise. A rectal
examination (PR) is mandatory and it is considered negligent not to perform this is a cauda
equine syndrome is missed. Urgent MRI is required to determine the level of prolapse and urgent
discectomy is required once the diagnosis is confirmed. Even with prompt surgical intervention,

55

a significant number of patients have residual nerve injury with permanent bladder and bowel
dysfunction.
RedFlagsymptoms&signs

Clinical evidence of cauda equina syndrome is one of the red flags for serious spinal disease.
Other symptoms of serious underlying pathology (tumour, infection, spondylolisthesis) should
be excluded when assessing someone with back pain.

Red flags include

1. Back pain in the younger patient (<20 years).

Significant back pain in childhood, adolescence or early adulthood is uncommon. Younger
children are more susceptible to infections (osteomyelitis, discitis) whilst adolescents are the
peak age for spondylolisthesis as well as some benign (eg osteoid osteoma) and malignant (eg
osteosarcoma) primary bone tumours. Clinicians should have a low index of suspicion for
referral or MRI.

2. New back pain in the older patient (>60 years).

Back pain in the older patient may represent arthritic change or a crush fracture. However
patients in this age group are at higher risk of neoplasia, particularly metastatic disease and
multiple myeloma.

3. Nature of pain constant, severe pain, worse at night

Mechanical back pain is worse with activity and tends to be relieved by rest. Pain from tumour or
infection tends to be constant, unremitting, severe and worse at night

4. Systemic upset

Fevers, night sweats, weight loss, fatigue and malaise may indicate the presence of underlying
tumour or infection.

Any suspicion of underlying infection or tumour requires thorough history and examination with
potential investigations including bloods (CRP, FBC, U&Es, bone biochemistry, plasma protein
electrophoresis, PSA for males, blood culture if suspecting infection), spine xray (may show
vertebral collapse of loss of a pedicle on AP view), chest xray, bone scan and MRI scan.

Neck
Cervicalspondylosis

As with the rest of the spine, spondylosis can occur with disc degeneration leading to increased
loading and accelerated OA of the facet joints. Patients will complain of slow onset stiffness and
pain in the neck which can radiate locally to shoulders and the occiput. Physiotherapy and
analgesics are the mainstay of treatment.

Osteophytes can also impinge on the exiting nerve roots resulting in a radiculopathy involving
the upper limb dermatomes and myotomes which may require decompression for severe
symptoms resistant to conservative management
Cervicaldiscprolapse

Acute and degenerative disc prolapse can also occur in the cervical spine producing neck pain
and potentially nerve root compression. With nerve root compression patients complain of
shooting neuralgic pain down a dermatomal distribution with weakness and loss of reflexes
depending on the nerve root affected. Typically, the lower nerve root is involved (ie C7 root for

56

C6/7 disc, C8 root for C7/T1 disc). A large central prolapse can compress the cord leading to a
myelopathy with upper motor neurone symptoms and signs.

Clinical findings and MRI will aid localisation of the affected level and again for cases resistant to
conservative management surgery may be considered (discectomy). As with lumbar disc
prolapse, the number of patients with asymptomatic disc prolapse increases with age resulting in
a higher rate of false positives on MRI scanning. Clinical findings should correlate with MRI
findings before contemplating surgery.
Cervicalspineinstability

Atraumatic cervical spine instability can occur in Down syndrome and rheumatoid arthritis

Children with Down syndrome are at risk of developing atlantoaxial (C1/C2) instability with
subluxation potentially causing spinal cord compression. Screening with flexionextension xrays
will demonstrate the abnormal motion (high atlantodens interval). Children with minor degrees
of instability may be prevented from high impact / contact sports. Severe instability or the
presence of abnormal neurology may require surgical stabilization.

In rheumatoid arthritis, atlantoaxial subluxation can also occur due to destruction of the
synovial joint between the atlas and the dens and rupture of the transverse ligament. Again
subluxation can result in cord compression which can be fatal. Less severe cases (seen on flexion
extension views) may be treated with a collar to prevent flexion whilst more severe cases may
require surgical fusion. Lower cervical subluxations can occur due to destruction of the synovial
facet joints and uncovertebral joints again with potential for cord compression (myelopathy)
with upper motor neuron signs (wide based gait, weakness, increased tone, upgoing plantar
response). Again measurements are taken from flexionextension xrays and more severe cases
may require stabilization/fusion.

57

Shoulder

The shoulder or glenohumeral joint is a ball and socket synovial joint formed by the humeral
head and the scapular glenoid. The shoulder girdle is formed by the scapula, the clavicle, the
proximal humerus and the supporting muscles including the deltoid and the muscles of the
rotator cuff. The shape of the glenohumeral joint and the complex interplay between bony
anatomy and the supporting muscles affords a wide range of movement. Due to the lack of
inherent bony stability, the shoulder joint is dependent on the surrounding musculature for
stability with the rotator cuff muscles providing an essential role.

The rotator cuff is formed by four muscles hold the humeral head in place at he same time as
providing a number of essential movements.

Supraapinatus
Infraspinatus
Teres Minor
Subscapularis

Figure 24: Rotator cuff muscles. 1=supraspinatus, 2=infraspinatus, 3=teres minor,

4=subscapularis. Source: Macdonald A (2011).

The supraspinatus, infraspinatus and teres minor muscles attach to the greater tuberosity.
Supraspinatus is responsible for initiation of abduction whilst infraspinatus and teres minor are
external rotators. Subscapularis attaches to the lesser tuberosity and is the principal internal
rotator.

Collectively the rotator cuff muscles serve the crucial function of pulling the humeral head into
the glenoid to provide a stable fulcrum for the powerful deltoid muscle to abduct the arm. The
rotator cuff muscles are under significant repeated stress and acute or degenerate tendon tears
can occur which can cause pain and disability. Furthermore due to altered shoulder
biomechanics, chronic rotator cuff insufficiency can lead to glenohumeral OA. The shoulder can
also be subject to primary OA of the glenohumeral and acromioclavicular joints and other soft
tissue disorders.

Shoulder problems tend to occur in different age groups. In the younger adult, instability is the
usual source of pain. In the middle aged, rotator cuff tears (grey hair, cuff tear) and frozen
shoulder are often the problem. In the elderly, glenohumeral OA becomes more likely.

58

Impingementsyndrome/Painfularcsyndrome

This is a syndrome where the tendons of the rotator cuff (predominantly supraspinatus) are
compressed in the tight subacromial space during movement producing pain. Typically the
patient has a painful arc between around 60 to 120 degrees of abduction (these values are
variable) as an inflamed area of supraspinatus tendon passes though the subacromial space.

Figure 25: Painful arc syndrome, occurs when an inflamed and swollen area of the supraspinatus
tendon passes beneath the acromioclavicular joint. Source: Dandy D and Edwards DJ (2009).
Causes include:

Tendonitis
Subacromial bursitis
Acromioclavicular OA with inferior osteophyte
A hooked acromion
Rotator cuff tear

Pain from impingement characteristically radiates to the deltoid and upper arm. Tenderness may
be felt below the lateral edge of the acromion. Hawkins test (internally rotating the flexed
shoulder) recreates the patients pain. Cervical radiculopathy should be excluded from history
and examination.

Treatment is conservative in the first instance with the majority of cases settling with NSAIDs,
analgesics, physiotherapy and subacromial injection of steroid. Up to 3 subacromial injections
may be required. Refractory cases may benefit from subacromial decompression surgery to
create more space for the supwhich can be done as an open procedure or with minimally
invasive arthroscopic techniques.
Rotatorcufftear

The tendons of the rotator cuff can tear due to a significant injury in the younger patient
(including shoulder dislocation) or they can occur with minimal or no trauma as a consequence
of degenerate changes in the tendons. A classic history is of a sudden jerk (eg holding a rail on a
bus which suddenly stops) with subsequent pain and weakness. At least 20% of over 60 year olds
have asymptomatic cuff tears due to tendon degeneration.

Tears can be partial or full thickness and usually involve suprapinatus. Large tears can extend
into subscapularis and infraspinatus. Weakness of initiation of abduction (supraspinatus),

59

internal rotation (subscapularis) or external rotation (infraspinatus) may be detected and

wasting of supraspinatus may be seen. Tears are confirmed on Ultrasound or MRI.

The optimal treatment for rotator cuff tears is controversial. Rotator cuff repair (open or
arthroscopic) with subacromial decompression can be performed in an attempt to
improve/maintain strength and to prevent subsequent arthritis from chronic cuff deficiency.
However the tendon is usually diseased and failure of repair occurs in around a third of cases.
Very large tears may be irrepairable and the tendon may be retracted too far. Many patients do
well with physiotherapy to strengthen up the remaining cuff muscles which can compensate for
the loss of supraspinatus. Subacromial injection may help symptoms. Overall the long term
results of rotator cuff surgery are not fully known.
Frozenshoulder(adhesivecapsulitis)

This is a disorder characterized by progressive pain and stiffness of the shoulder in patients
between 40 and 60, resolving after around 1824 months. Patients will initially complain of pain,
which will subside (after around 29 months) as stiffness increases (for around 412 months)
and then the stiffness gradually thaws out over time, usually with good recovery of shoulder
motion. The principal clinical sign is loss of external rotation (along with restriction of other
movements) which can also occur in OA, however OA tends to affect older patients.

The aetiology is unclear. Sometimes there is a history of an innocuous triggering injury but often
not. It may also occur after shoulder surgery. Diabetics are particularly prone and the condition
has also been associated with hypercholesterolaemia and Dupuytrens disease (similar thickened
fascial tissue is found histologically). The capsule and glenohumeral ligaments become inflamed
then thicken and contract.

Treatment in the majority of cases is conservative with the aim of relieving pain and to prevent
further stiffening while the condition resolves naturally. Physiotherapy and analgesics help.
Intraarticular (glenohumeral rather than subacromial) injections can help in the painful phase.
Once the pain has settled, if the patient cannot tolerate functional loss due to stiffness, recovery
can be hastened by manipulation under anaesthetic (MUA which tears the capsule) or surgical
capsular release (usually done arthroscopically) which divides the capsule leading to improved
motion.
Instability

Instability of the shoulder involves painful abnormal translational movement or subluxation
and/or recurrent dislocation.

2 types of patterns exist:
Traumaticinstability
Patients can experience a traumatic anterior dislocation which after reduction may settle and the
shoulder stabilizes with rest and a physiotherapy strengthening programme. Some shoulders do
not stabilize and develop recurrent dislocations or subluxations, often with minimal force. Age at
time of first dislocation predicts the likelihood of further dislocations with 80% redislocation
rate in under 20s and 20% redislocation rate in over 30s.

With recurrent dislocations in this group, a Bankart repair (open or arthroscopic) can stabilize
the shoulder by reattaching the labrum and capsule to the anterior glenoid which was torn off in
the first dislocation.

Atraumaticinstability
Patients with generalized ligamentous laxity (idiopathic, EhlersDanlos, Marfans) can have pain
from recurrent multidirectional (anterior, posterior or inferior) subluxations or dislocations.
Treatment is difficult as soft tissue procedures may not work.

60

Acutecalcifictendonitis

This condition results in the acute onset of severe shoulder pain and is characterized by calcium
deposition in the supraspinatus tendon which is seen on xray just proximal to the greater
tuberosity. Great relief of pain is achieved with subacromial steroid and local anaethetic
injection. The condition is selflimiting with pain easing as the calcification resorbs.

Othercausesofshoulderpain

Inflammation of the tendon of long head of biceps (biceps tendonitis) causes anterior shoulder
pain with pain on resisted biceps contraction. Surgical division of the tendon with or without
attachment to the proximal humerus may be required to relieve symptoms. The tendon can
spontaneously rupture resulting in relief of symptoms however some are left with a bunched up
biceps muscle (Popeye deformity).

Tears in the glenoid labrum where the long biceps tendon attaches (known as SLAP lesions) can
also cause pain. Diagnosis is difficult but may be identified on MRI arthrogram (contrast injected
into joint). Treatment is controversial biceps tenotomy may be enough or labral resection or
repair may help.

Remember also that neck problems can cause referred pain to the shoulder and that angina
pectoris and diaphragmatic irritation (biliary colic, hepatic or subphrenic abscess) can present
with shoulder pain.

61

CompressiveNeuropathies

In contrast to cervical nerve root compression, peripheral nerve compression neuropathies will
cause symptoms and signs affecting peripheral nerve sensory and motor territories rather than
dermatomal and myotomal distributions.
CarpalTunnelsyndrome


The carpal tunnel of the wrist is formed by the carpal bones and the flexor retinaculum. The
median nerve passes through the carpal tunnel along with 9 flexor tendons (FDS & FDP to 4
digits + FPL) with their synovial covering. Any swelling within the confines of the carpal tunnel
may result in median nerve compression. Although it may be idiopathic (most cases), it can occur
secondary to many conditions including rheumatoid arthritis (synovitis less space) and
conditions resulting in fluid retention pregnancy, diabetes, chronic renal failure,
hypothyroidism (myxoedema). Carpal tunnel syndrome can also be a consequence of fractures
around the wrist (especially a Colles fracture). With pregnancy the symptoms usually subside
after childbirth. Women are affected up to 8 times more than men.

Patients will present with parathesiae in the median nerve innervated digits (thumb and radial
2 fingers) which is usually worse at night, loss of sensation and sometimes weakness of the
thumb or clumsiness in the areas of the hand supplied by the median nerve (figure). On
examination there may be demonstrable loss of sensation and/or muscle wasting of the thenar
eminence (with chronic sever cases). Symptoms can be reproduced by performing Tinels test
(percussing over the median nerve) or Phalens test, holding the wrists hyperflexed (which
decreases space in the carpal tunnel. Nerve conduction studies confirm the diagnosis with
slowing of conduction across the wrist.

Conservative treatment includes the use of wrist splints at night to prevent flexion. Injection of
corticosteroid can also be used. Surgical carpal tunnel decompression involves division of the
transverse carpal ligament under local anaesthetic (one of the most commonly performed
surgical procedures).
CubitalTunnelSyndrome

This involves compression of the ulnar nerve at the elbow behind the medial epicondyle (funny
bone area). Patients complain of paraesthesiae in the ulnar 1 fingers and Tinels test is usually
positive. Weakness of ulnar nerve innervated muscles may be present including the 1st dorsal
interosseous (abduction index finger) and adductor pollicis. The later can be assessed with
Froments test. Compression can be due to a tight band of fascia forming the roof of the tunnel
(known as Osbornes fascia) or due to tightness at the intermuscular septum as the nerve passes
through or between the two heads at the origin of flexor carpi ulnaris.

Figure 26: Positive Froment's test on the left. Due to the weakness of adductor pollicis, patient
will compensate action by flexing flexor pollicis longus of the thumb to maintain grip strength.
Source: Dent J (2011)

62



Nerve conduction studies confirm the diagnosis and the patient may need surgical release of any
tight structures.

63

Elbow

The elbow joint describes the articulation between the humerus and the bones of the distal
forearm. It consists of the humeroulnar joint (responsible for flexion/extension) and the radio
capitallar joint (responsible supination/pronation along with the proximal and distal radioulnar
joints). The triceps muscle which inserts onto the olecranon process powers elbow extension
whereas the brachialis (inserting onto the coronoid process) and biceps (inserting onto the
bicipital tuberosity of the radius) muscles flex the elbow. Supination is performed by the biceps
and supinator muscles whereas pronation is performed by contraction of the pronator teres
muscle proximally and the pronator quadratus muscle distally. The common extensor origin
arises from the lateral epicondyle whilst the common flexor origin arises from the medial
epicondyle. The enthesis (attachment) of the common extensor and flexor origins can become
painful (known as an enthesopathy). This gives rise to the conditions of lateral and medial
epicondylitis. Whilst primary OA of the elbow is rare (OA is more commonly 2 to trauma), the
elbow is commonly affected in rheumatoid arthritis.
TennisElbowLateralepicondylitis

This can occur as a repetitive strain injury in tennis players and others whom regularly perform
resisted extension at the wrist. It can also be a degenerative enthesopathy (inflammation of the
origin or insertion of a tendon or ligament into bone). Pathology demonstrates microtears in the
common extensor origin. Clinical features include a painful and tender lateral epicondyle and
pain on resisted middle finger and wrist extension.

This is a selflimiting condition (usually resolves). Treatment involves a period of rest from the
activities that exacerbate the pain, physiotherapy, NSAIDs, steroid injections and use of a brace
(known as an elbow clasp). Ultrasound therapy is also used but its efficacy is unclear. Rarely
refractory cases may be offered surgical treatment which involves division and/or excision of
some fibres of the common extensor origin however has variable results.
GolferselbowMedialepicondylitis

Medial epicondylitis is a consequence of repeated strain or degeneration of the common flexor
origin. Medial epicondylitis is less common than its lateral counterpart.

Again this is a selflimiting condition with physio, rest & NSAIDs the mainstay of treatment.
Injection in this area carries a risk of injury to the ulnar nerve.
Arthriticelbow

Primary OA of the elbow is uncommon. The elbow is often involved in rheumatoid arthritis and
OA can occur after trauma (intraarticular fractures).

Artritic change at the radiocapitellar joint which has failed conservative management can be
treated with surgical excision of the radial head which affords good pain relief with minimal
functional limitation.

An elbow severely affected by RA or OA at the humeroulnar joint which is refractory to
conservative management can be treated surgically with a Total Elbow Replacement which has
reasonable long term results however lifting in these patients is restricted to 2.5kg
postoperatively.

64

Hands
DupytrensContracture

This is a proliferative connective tissue disorder where the specialized palmar fascia undergoes
hyperplasia with normal fascial bands forming nodules and cords progressing to contractures at
the MCP and PIP joints. Pathology involves proliferation of myofibroblast cells and the
production of abnormal collagen (type 3 rather than type 1). The skin of the hand may be
adherent to the disease fascia and puckered. Palpable nodules may be present. Contractures most
commonly affect the ring and little fingers. Approximately half of cases have bilateral
involvement.

Figure 27: Advanced case of Dupuytren's causing the finger to bend into the palm. Source:
American Society for Surgery of the Hand (2012).

Males are much more commonly affected (by around 10:1), it can be familial (inherited in an
autosomal dominant pattern) and has a high prevalence in those of Northern European /
Scandinavian descent. Dupytrens can also be seen as a feature of alcoholic cirrhosis and as a side
effect of phenytoin therapy. It is also more common in diabetics.

It can also occur with other fibromatoses including Peyronies disease and plantar fibromatosis
(Ledderhose disease). Young patients and patients with fibromatosis elsewhere tend to have
more aggressive forms of the disease.

Mild contractures may be tolerated but surgical treatment can be offered if contractures are
interfering with function. Up to 30 of contracture can be tolerated at the MCP joint and but the
PIPJ readily stiffens and any contracture here is usually an indication for surgery. Surgery
involves either removal of all diseased tissue (fasciectomy) or division of cords (fasciotomy).
Recurrence can occur particularly in the younger patient. Severe contractures (finger in palm)
may be most appropriately treated with amputation.
TriggerFinger

Tendonitis of a flexor tendon to a digit can result in nodular enlargement of the affected tendon,
usually distal to a fascial pulley over the metacarpal neck (the A1 pulley). Movement of the finger
produces a clicking sensation which may be painful and the finger may lock in a flexed position as
the nodule passes under the pulley but cant go back though on extension. The patient may have
to forcibly manipulate the finger to regain extension, usually with pain. Any finger can be affected
but the middle and ring are those most commonly affected.

In most cases injection of steroid around the tendon within the sheath will relieve symptoms.
Surgery can be offered in recurrent and persistent cases. Surgery involves incision of the pulley
to allow the tendon to move freely.

65

OAhand&wrist

Wear and tear arthritis in the small joints of the hand can be troublesome for patients
particularly when performing intricate tasks. 80% of over 60s will have radiological evidence of
OA in the hands but only a minority complaining of symptoms.

Distal interphalangeal joints (DIP) OA is very common in postmenopausal women. DIPs will
become painful, swollen and tender eventually affecting all fingers. Stiffness and bony thickening
can be seen readily on examination (Heberdens nodes). An associated dorsal ganglion cyst
(known as a mucous cyst) may be present. Mild to moderate OA may be treated with removal of
osteophytes and excision of any mucous cyst. For severe pain arthrodesis may be performed.

The proximal interphalangeal joint (PIP) can also be affected with OA and bony swelling
(Bouchards nodes). For the index finger arthrodesis may be required to preserve pinch grip. For
other fingers replacement arthroplasty may be required however results are variable and re
operation rates are high.

Figure 28: Heberdens nodes in DIP and Bouchards nodes in PIP. Source: American College of
Rheumatology (2011).

Rarely OA can affect the metocarpalphalageal (MCPs) joints but there is usually specific cause for
this. For example: previous injury, occupational stress, gout or infection. Surgical treatment is
possible for arthritis at the MCPs. MCP joint replacements are available which may relieve pain
and improve ROM however complications are not uncommon (ulnar drift, extensor tendon
subluxation).

The 1st carpometacarpal joint (trapziometacarpal joint) at the base of the thumb metacarpal is
commonly affected by OA, particularly in women with up to 1/3 of women over 40 having
radiographic signs present. Injection of steroid can help an acute flare up whilst excision
arthroplasty (trapeziectomy) or fusion may cure chronic pain.

The joints between the scaphoid, trapezium and trapezoid (STT joint) can be affected by primary
OA. Selected fusion of these carpal bones or wrist fusion may be required for severe symptoms.

OA of the radiocarpal joint of the wrist usually occurs as a consequence of trauma (eg scaphoid
nonunion, carpal dislocation). Wrist arthroplasty or fusion may be considered.
RAhands

The hands are the site where RA seems to cause the greatest number of problems and is most
visible. Patients with longstanding disease will eventually develop deformed, painful and
occasionally malfunctioning hands. RA tends to spare the DIPs (in contrast with OA and psoriatic
arthritis).

66

The natural history of disease in the hands can be thought of as occurring in three stages.

1. Synovitis and tenosynovitis inflammation within the joints and the tendon sheath lead
to swelling and pain in the affected structures.
2. Erosions of the joints inflammatory pannus denudes the joints of articular cartilage
3. Joint instability and tendon rupture following the progressive destruction of the bony
and soft tissue structure in the hand patients can progress to subluxation and chronic
tenosynovitis predisposes to extensor tendon ruptures.

Thankfully the end stages of RA are becoming less and less common due to the introduction of
modern disease modifying antirheumatic drugs (DMARDs). Nonetheless there is still a
significant population of people who will exhibit hand deformities as a result of the disease.
These deformities are easily identified on clinical examination.

Volar MCPJ subluxation
Ulnar deviation
Swan neck deformity (hyperextension at PIPJ with flesion DIPJ)
Boutonniere deformity (flexion at PIPJ with hyperextension at DIPJ)
Z thumb

Figure 29: Swan neck deformity and Boutonniere deformity in RA. Source: Douglas G et al.
(2009).
Tenosynovectomy (excision of synovial tendon sheath) may prevent tendon rupture. When
extensor tendons to the wrist or fingers rupture direct surgical repair is not possible as repair of
the diseased tendon will fail. Tendon transfers or joint fusions may be required to preserve
function.

Soft tissue releases (lengthening) may be required for contractures whilst MCP replacements, PIP
replacements or fusions, wrist replacement or fusion may be required for severe arthritic change.

Resection of the distal ulna may be required for DRUJ arthritis.

A multidisciplinary approach is required for the management of RA with rheumatologists,
orthopaedic surgeons, physiotherapists, occupational therapists and orthotists all having a role
in improving symptoms and maintaining function.

Ganglioncyst

These are common mucinous filled cysts found adjacent to a tendon or synovial joint. They are
common in the hand (DIPJ mucous cyst, flexor tendon) and wrist (dorsal or volar). They can
also occur in the foot and ankle as well as the knee (Bakers cyst).

They can case localized pain and many patients wish to have them to be removed for cosmetic
reasons. The cysts are firm, smooth and rubbery and should transilluminate. Needle aspiration

67

may be attempted (watch volar ganglion radial artery) however recurrence is common (50
70%). Surgical excision may be required if the swelling causes localized discomfort. The historic
treatment of striking the wrist with a heavy book (bible technique) to burst the swelling is not
advised.

Giantcelltumouroftendonsheath

These are the second most common soft tissue swellings of the hand (after ganglions). They are
usually on the palmar surface especially around the PIP joint of the index and middle fingers and
are typically well circumscribed but can be diffuse. They may or may not cause pain, they can
envelop the digital nerve or artery and they can erode into bone. Histologically they contain
multinucleate giant cells and haemosiderin (which gives their brown appearance). Excision is
usually recommended to prevent local spread and to treat symtoms. Recurrence is not
uncommon (1020%).

68

Hip


Hip pathology typically produces pain in the groin which may radiate to the knee (due to the
obturator nerve supplying both joints and referred pain). Hip pathology may also result in
buttock pain however lumbar spine and SI joint problems can also give rise to buttock pain. Hip
pathology can also present purely with knee pain, particularly in SUFE.

Examination may reveal a reduced range of motion with loss of internal rotation usually the first
sign. Pain may be exacerbated by rotational movements. With altered hip biomechanics or
weakness from chronic disuse, abductor weakness (gluteus medius & minimus) may manifest as
a positive Trendellenburg sign or Trendellenburg gait. Shortening of the lower limb may also be
seen in severe OA, Perthes, SUFE or AVN (or fracture).

Groin pain can also be due to a hernia (inguinal or femoral), tendonitis (especially adductor
tendoinitis), pubic symphysis dysfunction or a high lumbar disc prolapse (with L1/2
radiculopathy, rare).
HipArthritis&TotalHipReplacement(THR)

Surgery for primary OA or arthritis due to RA, seronegative inflammatory arthropathy, AVN,
dysplasia, Perthes or SUFE usually involves Total Hip Replacement (THR).

THR is widely considered one of the most successful operations in modern surgery with the first
successful hip replacement designed by Sir John Charnley in the 1960s whose pioneering low
friction arthroplasty used a stainless steel stem with a small head (to reduce wear) and a high
density polyethylene cup with both components being cemented in place using a bone cement
(PMMA) which had previously only been used in dentistry. Today, the cemented
metal/polyethylene THR remains the gold standard.

Any THR will ultimately fail as a result of loosening of one or both of the prosthetic components.
In a low demand older patient, one can expect the cup of a hip replacement to last around 15
years and the stem to last over 20 years before failure from wear or loosening. Less than 5% of
implants loosen before ten years. The use of cement was historically blamed for loosening
however this has proven not to be the case. Uncemented components are widely used with the
aim of bone growing into a roughened porous surface however no uncemented component has
proven to give superior clinical results than cemented components.

Loosening of components is predominantly due to wear particles from the bearing surface
causing an inflammatory response at the implantbone (or cementbone) interface. Macrophages
ingest microscopic wear particles and release inflammatory mediators resulting in osteoclastic
bone resorption. Alternatives to the metal/polyethylene bearing have been developed in an
attempt to reduce wear and loosening. Ceramics are now widely used as they have favourable
friction properties. Historically they were too brittle and failed due to fatigue but toughened
ceramics are now used by many surgeons. The long term effects are not fully known. Metalon
metal hip replacements were designed (including hip resurfacing with a metal cap for the
femoral head avoiding the use of a stem) however there are concerns in a minority of cases of
local reaction to metal debris resulting in an inflammatory pseudotumour which can cause
necrosis of muscle and bone. Harder, smoother polyethylene has also been developed.

The decision to undergo THR is dependent on the level of pain and disability which the patient
experiences. Conservative measures include simple analgesics, physiotherapy, use of a stick
(which reduces the joint force by 15%), weight reduction and modification of activities. If
conservative measures are failing to control symptoms, THR may be considered.

The patients level of pain can be gauged by asking about analgesic use, rest pain and sleep
disturbance. Disability can be determined by asking about walking distance, activities of daily
living (dressing, bathing etc.) and the impact of the arthritic hip on any hobbies.

69

As with any other surgical procedure, the patient journey through surgery as well as the risks
and benefits of the procedure are explained as part of the consenting process.

Early local complications include infection, dislocation, nerve injury (sciatic nerve) and leg length
discrepancy. Early general complications include medical complications from surgery (MI, chest
infection, UTI, blood loss & hypovolaemia) as well as deep vein thrombosis and pulmonary
embolism (around 0.5% incidence). Late local complications include early loosening, late
infection (haematogenous spread from a distant site) and late dislocation (due to component
wear).

When a hip replacement has failed, it can be redone (known as a revision hip replacement)
however this involves bigger and more complex surgery than a first time (primary) procedure
with often substantial blood loss, around twice the complication rates and often poorer
functional outcome. Additionally, revision hip replacements tend not to last as long as primary
hip replacements.

There are implications of performing THR in younger patients as they have a higher risk of
requiring revision surgery later in life as they will put more demand on their prosthetic hip than
an elderly patient and they have a longer life expectancy. This is the rationale behind delaying
surgery for as long as possible however if the patients pain and disability is severe, hip
replacement in the younger patient may be justified.
AVNofthehip

The hip joint is one of the commonest sites of AVN which as previously discussed may be primary
/ idiopathic or 2 to alcohol abuse, steroids, hyperlipidaemia or thrombophilia. Again patients
tend to present with groin pain.

Early cases may only show changes on MRI (preradiographic AVN) whilst later cases show
patchy sclerosis of the weight bearing area of the femoral head with a lytic zone underneath
formed by granulation tissue from attempted repair. The lytic zone gives rise to the classic
hanging rope sign on Xray. The femoral head may then collapse with irregularity of the
articular surface and subsequent secondary OA.

If the condition is detected early enough (precollapse), drill holes can be made up the femoral
neck and into the abnormal area in the head in an attempt to relieve pressure (decompression),
promote healing and prevent collapse. Once collapse has occurred, the only surgical option is
THR.
Trochantericbursitis/glutealcuffsyndrome

The broad tendinous insertion of the abductor muscles (predominantly the gluteus medius) is
under considerable strain and is subject to tendonitis and degeneration leading to tendon tears.
The trochanteric bursa can also become inflamed. The condition is similar to rotator cuff
problems of the shoulder.

Patients have pain and tenderness in the region of the greater trochanter with pain on resisted
abduction.

Treatment is with analgesic, antiinflammatories, physiotherapy (to strengthen other muscles
and avoid abductor weakness) and steroid injection. No surgical treatment has a proven benefit.

70

Knee

The knee joint consists of the medial and lateral compartments of the tibiofemoral joint and the
patellofemoral joint. Although these joints are often considered separately, they all
communicate with each other as one synovial joint. The surfaces are covered with hyaline
cartilage with the retropatellar surface having the thickest hyaline cartilage in the body (a
reflection of the load placed on the patella especially descending stairs.

The tibiofemoral joint contains the fibrocartilaginous menisci which ensure congruence between
the concave femoral condyles and the flattish tibial plateau. The menisci are important shock
absorbers and act to distribute load evenly.

The four main ligaments include the anterior cruciate ligament (ACL), the posterior cruciate
ligament (PCL) and the two collateral ligaments the medial (MCL) and lateral (LCL) collateral
ligaments.

The principal role of the ACL is to prevent abnormal internal rotation of the tibia (although it is
clinically tested by assessing anterior translation of the tibia). The PCL prevents hyperextension
and anterior translation of the femur (although it is tested by assessing posterior translation of
the tibia). The MCL resists valgus force whilst the LCL resists varus force and abnormal external
rotation of the tibia.
KneearthritisandKneereplacement

Early OA of the knee may be predisposed by previous meniscal tears, ligament injuries
(especially ACL deficiency) and malalignment (genu varum medial OA, genu valgum lateral
OA). Arthritis may also be due to seropositive and seronegative inflammatory arthritis. Many
cases of OA are primary OA with no obvious causative factor. Primary knee OA may have
genetic influences and hobbies (eg football, distance running) or occupation may play a role
however this has not been conclusively proven. Patellofemoral dysfunction and instability
predispose to the development of patellofemoral OA.

Younger patients with isolated medial compartment OA, particularly in varus knees may be
helped by an osteotomy of the proximal tibia (known as a high tibial osteotomy, HTO) to shift
load to the lateral compartment. This may be particularly useful for heavy manual workers (eg
builders) as a knee replacement would fail early if subject to such heavy work. However, the
results of osteotomy are less predictable than knee replacement and benefit only lasts around 7
10 years. Moreover the results of knee replacement after osteotomy are inferior to those in the
unoperated knee.

Knee replacement can be considered in a patient with substantial pain and disability where
conservative management is no longer effective. Knee replacements can resurface all 3
compartments of the knee (total knee replacement, TKR) or be a partial knee replacement
(unicompartmental knee replacement, UKR or patellofemoral replacement).

UKR has been proposed as a potential treatment for patients with isolated OA of the medial or
lateral compartment as a less invasive surgery with less bone removal and preservation of the
knee ligaments. It has been advocated particularly for use in the younger patient. If failure
occurs, revision to a TKR can be performed. Patellofemoral replacement has been proposed for
isolated PFJ OA. The failure rate of partial knee replacement is higher than for TKR particularly as
arthritis can progress in the unresurfaced compartments. It remains unclear if they provide any
benefit over conventional TKR.

TKR is a surface replacement with short stems or no stems used. Most components are cemented.
The femoral component is usually cobalt chrome alloy or stainless steel (low friction metal
alloys), the tibial component is cobalt chrome, stainless steel or titanium with a high density
polyethylene bearing surface. It is controversial whether a replacement patellar button is
required as the results are equivalent with or without. The ACL is usually excised and with many
designs the PCL is also sacrificed.

71


The success of TKR is related to the accuracy of component alignment and the tension of the
surrounding soft tissue envelope. Component malalignment and unequal tension of the collateral
ligaments may produce asymmetric stress between the medial and lateral compartments with
potential for component loosening due to mechanical stress or wear of the polyethylene bearing
with subsequent faitigue failure or loosening from osteolysis. Tight collateral ligaments need to
be lengthened / released for symmetric distribution of forces but if they are too slack, the patient
may experience instability.

The risks of surgery are similar to hip replacement in terms of infection rates, thrombosis and
medical complications. Whilst there is very little risk of joint dislocation compared with hip
replacements, there is a higher chance of unexplained pain after TKR (around 15% have
moderate pain compared to 510% of THR). This may be due to the complexity of and reliance
upon the tension of the soft tissues around the knee (whereas the hip is not so reliant on soft
tissue tension).

Again there are serious implications of performing knee replacement in the younger patient as
they have a higher likelihood of requiring revision surgery with a higher risk of early failure.
Revision TKR is a bigger undertaking than primary TKR often requiring the use of stems and the
use of a more hinged type of knee implant. The results of revision surgery are generally inferior
to those of primary TKR.
Softtissueinjuriesoftheknee

As with most clinical presentations in medicine, the diagnosis of knee injuries can usually be
found by detailed history taking with confirmation by clinical examination and subsequent
investigation.

Meniscal injuries classically occur with a twisting force on a loaded knee (eg turning at football,
squatting). The patient localizes pain to the medial (majority) or lateral compartment and
an effusion develops by the following day. The patient then complains of pain and usually has
mechanical symptoms either a catching sensation or locking where they have difficulty
straightening the knee with a 15 or so block to full extension. Patients knees may feel about to
give way if a loose meniscal fragment is caught in the knee when walking.

ACL ruptures usually occur with a higher rotational force, turning the upper body laterally on a
planted foot (leading to internal rotation force on the tibia), often at football, rugby, skiing or
another high impact sport. A pop is usually felt or heard and the patient usually develops a
haemarthrosis with swelling (usually tense) within an hour of the injury and deep pain in
the knee. The patient may then complain of rotatory instability with their knee giving way
when turning on a planted foot (due to excessive internal rotation of the tibia).

Valgus stress injuries (eg rugby tackle from the side) will usually tear the MCL with higher
forces also potentially damaging the ACL and risking lateral tibial plateau fracture.

A direct blow to the anterior tibia with the knee flexed (eg motorcycle crash) or hyperextension
may rupture the PCL whilst hyperextension.

A varus stress injury may rupture the LCL +/ PCL.

The knee can be difficult to examine in the aftermath of an injury as pain and apprehension may
limit examination findings and
Meniscaltears

In younger patients, meniscal tears usually occur due to a sports related injury. Note also that
around 25% of acute ACL ruptures also have a meniscal tear. History findings with a torn
meniscus are detailed above. Clinical examination may reveal an effusion, joint line tenderness
and pain on tibial rotation localizing to the affected compartment. A locked knee with a displaced

72

bucket handle meniscal tear will have a 15 or so springy block to full extension. MRI will confirm
the clinical suspicion.

Medial meniscal tears are approximately 10 times more common than lateral meniscal tears due
to the fact that the medial meniscus is more fixed and less mobile than the lateral meniscus and
the force from pivoting movements is centred on the medial compartment.

Meniscal tears can have various patterns including longitudinal tears, radial tears, oblique tears
and horizontal tears. Large longitudinal tears may result in a bucket handle tear where a large
meniscal fragment is able to flip out of its normal position and displace anteriorly or into the
intercondylar notch where the knee locks and is unable to fully extend due to mechanical
obstruction from the trapped meniscal fragment.

Degenerate meniscal tears can occur as the meniscus weakens with age. The meniscus can tear
spontaneously or with a seemingly innocuous injury. Degenerate tears tend to have complex
patterns with horizontal, longitudinal and radial components. Degenerate tears are probably the
first stage in many cases of knee osteoarthritis.

The meniscus only has an arterial blood supply in its outer third and therefore has limited
healing potential. Healing potential also decreases with age (over about 2530 years of age
healing rates are poor) and with increased time from the injury. Only reasonably fresh
longitudinal tears involving the outer 1/3 of the meniscus in a younger patient should be
considered for meniscal repair which involves suturing the meniscus to its bed. Even with careful
patient selection a relatively high proportion (around 25%) of meniscal repairs fail requiring
arthroscopic menisectomy.

Figure 30: Meniscal tears can be classified into 2 types based on vascular zones (A) or
appearance (B). The red zone has the highest potential for meniscal healing whereas the white
zone has essentially no potential for healing without enhancement. Source: Miller MD (2012).
More than 90% of meniscal tears are not suitable for repair. Whilst meniscal tears do not usually
heal, the pain and inflammation may settle with time, particularly with degenerate meniscal
tears. The knee can also smooth off its own meniscus given time. Steroid injection in
degenerate tears may help symptoms in the early period. If the pain or mechanical symptoms do
not settle within around 3 months then arthroscopic partial menisectomy can be performed with
around 7080% improvement in symptoms. Knees with degenerate changes on xray (loss of joint

73

space, sclerosis, osteophytes) or MRI (hyaline cartilage loss, bone marrow oedema) are unlikely
to benefit from arthroscopic menisectomy as removal of meniscal tissue may increase the stress
on already worn / damaged surfaces.
ACLrupture

Relevant history from an ACL rupture has been discussed. The principal complaint of ACL
deficiency is rotatory instability with giving way on turning. Clinical examination with reveal
knee swelling (haemarthrosis or effusion) with excessive anterior translation of the tibia on the
anterior drawer test and Lachman test. (Rotatory subluxation may also be demonstrated by the
pivot shift test however this needs a relaxed patient and can cause pain and therefore should
probably only be performed by a specialist).

ACL ruptures may cause little or no problems in some, whilst in others they can give substantial
problems with function. Approximately 1/3 of patients will compensate well and do whatever
they please (including sports), 1/3 will manage by avoiding certain movements but may not be
able to do high impact sports and 1/3 will do poorly with frequent giving way even with normal
daily activities. Physiotherapy to strengthen give proprioceptive training to the quadriceps and
hamstrings muscles may help compensation. Older patients are more likely to compensate or
cope with their ACL deficient knee.

Primary repair of the torn ACL is not effective and overall around 40% of patients with ACL
rupture end up having a reconstruction. Professional sportsmen or women who need to get back
to their profession as quick as possible usually proceed straight to ACL reconstruction and those
whose knees give way on sedentary activity or those who have a strong desire to get back to high
impact sport but cannot do so despite physiotherapy are good candidates for ACL reconstruction.

ACL reconstruction involves tendon graft (usually patellar tendon or semitendinosis & gracilis
autograft) being passed through tibial and femoral tunnels at the usual location of the ACL in the
knee and secured to the bone. Intensive rehabilitation is required and it may take up to a year to
get back to high impact sports.

MCLtears

MCL injuries are fairly common however the MCL is a fairly forgiving knee ligament with healing
expected in the majority of partial and complete tears and little or no instability. Patients may
have laxity and pain on valgus stress with tenderness over the origin or insertion of the MCVL.
Acute tears are usually treated in a hinged knee brace. Chronic MCL instability can be treated
with MCL tightening (advancement) or reconstruction with tendon graft.
PCLrupture

PCL rupture in isolation is not common. PCL reconstruction is usually performed for
reconstruction of the multiple ligament injured knee. With isolated PCL rupture only those with
severe laxity and recurrent instability with frequent hyperextension or feeling unstable
descending stairs (with anterior subluxation of the femur) are considered for surgical
reconstruction (usually with cadaveric achilles tendon allograft).
LCLrupture

Treatment of LCL ruptures is usually surgical with early repair or late reconstruction with
tendon graft. Patients usually have marked instability on rotational movement (excessive
external rotation of the tibia and varus).

The hyperextension and varus giving rise to the injury also gives a high incidence of common
peroneal nerve injury from excessive stretch. LCL injuries are often part of multiple ligament
knee injuries with a high incidence of vascular injury (popliteal artery intimal or complete tear).

74

Combinedkneeligamentruptures&kneedislocation

With higher degrees of force, some injuries can involve rupture of more than one of the four knee
ligaments.

Multiligament knee injuries often require surgical reconstruction due to the degree of instability.

Complete knee dislocations result in rupture of all four of the knee ligaments and have a high
incidence of neurovascular injury. They should be reduced as an emergency and may require
external fixation for temporary stabilization. Intimal tears can occur which later thrombose and
therefore regular checks on the circulation of the foot are mandatory. Any concern with the distal
circulation mandates a vascular surgery assessment and vascular stenting or bypass may be
required. Reperfusion may result in compartment syndrome especially after prolonged
ischaemia and fasciotomies may be necessary. Patients usually require multiple ligament
reconstruction.
Osteochondralandchondralinjuries

These occur due to impaction or shear of the articular surfaces or due to a direct blow. Ongoing
pain and effusion after a knee injury warrants further investigation. Assessment is performed
with Xray, MRI and with arthroscopy. Acute injuries involving large osteochondral fragments
with a substantial proportion of bone should be fixed with pins. If they are from a nonweight
bearing area or have little bone attached they are usually removed arthroscopically.

The defect in the surface of the knee may fill in with fibrocartilage (scar type hyaline cartilage)
which is not as good as hyaline cartilage but performs a reasonable job. If a defect has bare bone
at its base it can be drilled or holes made to induce bleeding (known as microfracture) to
promote fibrocartilage formation from stem cells differentiating into chondroblasts. Other
techniques include taking osteochondral plugs from nonweight bearing areas and plugging them
into the defect (known as moasaicplasty) and culturing chondrocytes from a sample of hyaline
cartilage on a biological membrane and suturing this onto the defect. Clinical results of these
more complex techniques suggest no benefit over the simpler microfracture technique.
Extensormechanismruptures

The patellar tendon or quadriceps tendon can rupture with rapid contractile force which can
occur after lifting a heavy weight, after a fall or spontaneously in a severely degenerate tendon.
Patellar tendon ruptures tend to occur in a younger age group (<40) with quadriceps tendon
rupture in older patients (over 40).

Predisposing factors include history of tendonitis, chronic steroid use or abuse (body builders),
diabetes, rheumatoid arthritis and chronic renal failure. Quinolone antibiotics (eg ciprofloxacin)
can cause tendonitis and can risk tendon ruptures. Steroid injections for tendonitis of the
extensor mechanism of the knee should be avoided due to high risk of tendon rupture.

The assessment of any acute knee injury should include the Straight Leg Raise Test (SLR)
to determine if the extensor mechanism is intact. Any doubt requires specialist
assessment and investigation. Patients will also usually have an obvious palpable gap in the
extensor mechanism and Xrays may reveal a high (PT rupture) or low lying (quads rupture)
patella. Partial tears can also occur which may have some extensor mechanism function but
reduced power. In obese patients the gap may not be obvious and ultrasound may determine the
extent of the injury.

In clinically obvious cases or with ultrasound confirmation, the treatment of complete and
substantial partial tears is surgical with tendon to tendon repair or reattachment of the tendon to
the patella.
Patellofemoraldysfunction

75

Patellofemoral dysfunction describes disorders of the patellofemoral articulation resulting in

anterior knee pain. It encompasses and in many cases is synonymous with various diagnoses
including chondromalacia patellae (softening of the hyaline cartilage), adolescent anterior knee
pain and lateral patellar compression syndrome.

The pull of the quadriceps muscle tends to pull the patella in a slight lateral direction. In some
people, excessive lateral force produces anterior knee pain and the lateral facet of the patella is
compressed against the lateral wall of the distal femoral trochlea. Patellofemoral dysfunction is
commoner in females (due to wider hips resulting in a more lateral pull of the quadriceps,
particularly during adolescence (due to a greater degree of ligamentous laxity). Other pre
disposing factors include joint hypermobility, genu valgum and femoral neck anteversion.

Patients tend to complain of anterior knee pain, worse going downhill, a griniding or clicking
sensation at the front of the knee and stiffness after prolonged sitting causing pseudolocking
where the knee acutely stiffens in a flexed position (in contrast to true locking from a bucket
handle meniscal tear).

The vast majority (at least 90%) of sufferers improve with physiotherapy aimed at rebalancing
the quadriceps muscles (specifically strengthening vastus medialis obliquus, VMO). Taping may
alleviate symptoms. Surgery is a last resort with about a 70% success rate and may involve either
releasing a tight lateral retinaculum or if there is a relatively lateralized tibial tubercle, a tibial
tubercle transfer to aid patellar tracking.
Patellarinstability

Patellar dislocation can occur with a direct blow or sudden twist of the knee. The patella virtually
always dislocates laterally and may spontaneously reduce or require to be manually manipulated
back into position.

When the patella dislocates, the medial patellofemoral ligament tears and osteochondral fracture
may occur as the medial facet of the patella strikes the lateral femoral condyle which may be
suggested by a small opacification on Xray. A lipohaemarthrosis occurs with characteristic Xray
appearance. Predisposing factors include ligamentous laxity, female gender, shallow trochlear
groove, genu valgum, femoral neck anteversion and a high riding patella (patella alta).

The risk of recurrent instability decreases with age and physiotherapy to strengthen the
quadriceps may help. The risk of recurrent dislocation after first time dislocation is around 10%.

If recurrent dislocation is frequent, tibial tubercle transfer or medial patellofemoral ligament
(MPFL) reconstruction with tendon autograft may help.

76

FootandAnkle

AnkleOAarthrodesisandreplacement

Ankle OA may be idiopathic / primary OA or as a consequence of previous injury. Football
players are particularly prone to ankle OA.

Repeated dorsiflexion may result in anterior damage with osteophyte formation. Anterior
osteophytes may cause pain during dorsiflexion resulting in impingement. Pain on dorsiflexion
may be improved with removal of the anterior osteophytes (known as cheilectomy).

For patients with significant pain from advanced ankle OA, two surgical options exist
arthrodesis and ankle replacement. Ankle replacement may afford better functional outcome
due to some preservation of motion. The trouble with ankle replacements is that substantial
compressive and shearing force is placed across the relatively small bones and fixation of
implants to the distal tibia and talus can be a problem with (historically) higher rates of early
loosening, component sinkage and failure than hip or knee replacement. Contemporary ankle
replacements however have demonstrated survivorship of up to 90% at 10 years. Ankle
replacements should be reserved for elderly patients as once failure occurs, patients usually
require fusion which produces a shortened limb. Major malalignment is a contraindication to
ankle replacement.

Ankle arthrodesis is perhaps a more reliable option than ankle replacement as the need for
further surgery is much less and reoperation rates are lower. Typically fusion rates of around
80% are expected. Ankle arthrodesis and ankle replacements provide equivalent pain relief.
HalluxValgus

Hallux valgus is a deformity of the great toe due to medial deviation of the 1st metatarsal and
lateral deviation of the toe itself. The aetiology is poorly understood.

Figure 31: Hallux valgus with bunion. Source: Douglas G et al. (2009).
The condition is commoner in females (by up to 4:1) and there is often a familial tendency (but
no direct genetic link). The incidence increases with age however it can occur in adolescence. The
wearing of footwear has been implicated (the incidence is lower in populations who dont wear
shoes) but no evidence exists that tight shoes or high heels are to blame). Hallux valgus is
commoner in rheumatoid arthritis and other inflammatory arthropathies as well as some
neuromuscular diseases (multiple sclerosis, cerebral palsy).

The condition may be painful due to joint incongruence and a widened forefoot may cause
rubbing of the foot with shoes resulting in an inflamed bursa over the medial 1st metatarsal head

77

 a bunion. The great toe and second toe may rub causing ulceration and skin breakdown. In
severe cases the hallux may override the second toe.

Conservative treatment includes the wearing of wider and deeper accommodating shoes to
prevent painful bunions and the use of a spacer in the first web space to stop rubbing between
the great and second toes. Many patients want surgery to improve the appearance of their foot as
well as to improve symptoms. Surgical management involves osteotomies to realign the bones
and soft tissue procedures to tighten slack tissues and release tight tissues. Any surgery may
alter the complex biomechanics of the foot and overall around 30% of patients are dissatisfied
with their surgery. Some patients complain of pain in the metatarsal heads (metatarsalgia) after
surgery. Numerous surgical techniques have been described with no single procedure proving
ideal for all cases.
Halluxrigidus1stMTPJOA

Hallux rigidus is OA of the first MTPJ. It can be primary (degenerative) or secondary to
osteochondral injury.
Conservative treatment may involve the wearing of stiff soled shoe to limit motion at the MTPJ. A
metal bar can be inserted into the sole of a shoe. In early cases where dorsal osteophytes impinge
during dorsiflexion, removal of osteophytes (cheilectomy) may help.

The gold standard surgical treatment is arthrodesis. Successful fusion should alleviate pain with
the small sacrifice of no motion (the toe is usually pretty stiff anyway). Arthrodesis prevents
women wearing high heels. 1st MTP joint replacements including ceramic total joint
replacements and metal hemiarthroplasties are in use but the failure rates are quite high and
once failure occurs, salvage surgery is difficult and results are usually disappointing.
MortonsNeuroma

Plantar interdigital nerves (from the medial and lateral plantar nerves) overlying the
intermetatarsal ligaments can be subjected to repeated trauma. Irritated nerves can become
inflamed and swollen (forming a neuroma). Patients complain of a burning pain and tingling
radiating into the affected toes. Women are four times more commonly affected and the wearing
of high heels has been implicated as a cause. The third interspace nerve is most commonly
involved followed by the second.

Figure 32: Morton's neuroma is commonly found between the third and fourth metatarsals.
Source: Miller MD (2012).

78



Clinical examination may reveal loss of sensation in the affected web space and mediolateral
compression of the metatarsal heads may reproduce symptoms or produce a characteristic click.

Conservative management involves the use of a metatarsal pad or offloading insole. Steroid and
local anaesthetic injections may relieve symptoms and aid diagnosis. Ultrasound may be used for
diagnosis by demonstrating a swollen nerve. A neuroma can be excised however some patients
continue to experience pain and there is a small risk of recurrence.
Stressfracture

Metatarsal stress fractures most commonly occur in the 2nd metatarsal followed by the 3rd. They
may occur in runners, in soldiers on prolonged marches, in dancers or during distance walking in
people not conditioned or used to prolonged walks.

Xrays may not demonstrate a fracture for around 3 weeks until resorption at the fracture ends
occurs or callus begins to appear. Bone scan may be useful to confirm the diagnosis. Prolonged
rest for 612 weeks in a rigid soled boot is required to allow healing and resolution of symptoms.
AchillesTendonitisandRupture

Tendonitis of the Achilles tendon can occur due to repetitive strain (from sports) which leads to a
peritendonitis or due to degenerative process with intrasubstance microtears. Quinolone
antibiotics (ciprofloxacin etc), rheumatoid arthritis, other inflammatory arthropaties and gout
may also predispose to tendonitis. Pain can be in the main substance of the Achilles tendo or at
its insertion in the calcaneus.

Treatment is rest, physiotherapy conditioning, use of a heel raise to offload the tendon and use of
a splint or boot. Resistant cases may benefit from tendon decompression and resection of
paratenon however scars in this area can be problematic and the condition is usually self
limiting.

Tendonitis predisposes to tendon rupture. Steroid injection should not be administered
around the Achilles tendon due to risk of rupture.

Tendon rupture usually occurs in middle aged or older groups and is usually due to degenerative
changes within the tendon or recent tendonitis. Sudden deceleration with resisted calf muscle
contraction (eg lunging at squash) leads to sudden pain (like being shot in the back of the leg)
and difficulty weight bearing. Weakness of plantar flexion and a palpable gap in the tendon are
usually apparent. No plantarflexion of the foot is seen when squeezing the calf (Simmonds test).
Treatment remains controversial, with some advocate the suture repair of the damaged tendon
to restore the tension of the tendon more accurately and repair may have a slightly lower re
rupture rate. Repair is protected by around 8 weeks in a series of casts. Again wound problems
can occur with surgery and can be very problematic if healing does not occur. Many surgeons
recommend nonoperative management simply with a series of casts (again over 8 weeks or so)
if the gap in the tendon closes on plantarflexion. This avoids the potential for wound problems
and good functional outcome can usually be expected.
Plantarfasciitis

This is another selflimiting repetitive stress / overload or degenerative condition of the foot.
Pain with walking is felt at the origin of the plantar aponeurosis on the distal plantar aspect of
the calcaneal tuberosity with localized tenderness. Diabetes, obesity and frequent walking on
hard floors with poor cushioning in shoes may be causative factors. The cushioning heel fat pad
atrophies with age.

Rest, Achilles and plantar fascia stretching exercises and a gel filled heel pad may help.
Corticosteroid injection may also alleviate symptoms. Symptoms can take up to two years to

79

resolve. Surgical release of the plantar fascia is of dubious value and risks injury to the plantar
nerves.
Flatfoot

Flat feet can be a normal variation affecting up to 20% of the population where the medial arch
does not develop in childhood. It may have a familial tendency. Patients with generalized
ligamentous laxity are more likely to have flat feet. Developmental flat feet do not usually result
in any problems and do not require any specific treatment. Flat footed people may be at higher
risk of tendonitis of the tibialis posterior tendon.

Acquired flat foot may be due to tibialis posterior tendon stretch or rupture, rheumatoid arthritis
or diabetes with Charcot foot (neuropathic joint destruction).
Tibialisposteriortendondysfunction

The tibialis posterior tendon inserts predominantly onto the medial navicular and serves to
support the medial arch of the foot (as well as being a plantarflexor and invertor of the foot). The
tendon is under repeated stress and particularly with degeneration can develop tendonitis,
elongation and eventually rupture. Synovitis form RA can also result in tendon rupture.

Tendonitis should be treated with a splint with a medial arch support to avoid rupture. If this
fails to settle symptoms, surgical decompression and tenosynovectomy may prevent rupture.
Elongation or rupture leads to loss of the medial arch with valgus of the heel. Subsequent
degenerative OA of the hindfoot and midfoot may occur. If the foot remains supple with no OA
present, a tendon transfer may be performed to try to prevent secondary OA with a calcaneal
osteotomy to reduce stress often performed. Once OA ensues, the most appropriate surgical
treatment if symptoms are severe is arthrodesis.
Pescavus

Pes cavus is an abnormally high arch of the foot. It can be idiopathic but is often related to
neuromuscular conditions including Hereditary Senory and Motor Neuropathy, cerebral palsy,
polio(unilateral) and spinal cord tethering from spina bifida occulta. Claw toes often accompany
pes cavus. Its development is poorly understood.

Figure 33: Clinical apperance of pes cavus with claw toes. Source: Sugathan HK and Sherlock DA
(2009).
Pain from pes cavus may be treated with soft tissue releases and tendon transfer (lateral transfer
of tibialis anterior) if supple, or calcaneal osteotomy if more rigid. Severe cases may require
arthrodesis.

80

Clawandhammertoes

Claw toes and hammer toes occur due to acquired imbalance between the flexor and extensor
tendons. Claw toes have hyperextension at the MTPJ with hyperflexion at the PIPJ and DIP.
Hammer toes are similar but have hyperextension at the DIPJ.

Claw and hammer toes can be painful and can rub on footwear causing corns and skin
breakdown. Toe sleeves and corn plasters can prevent skin problems. Surgical solutions
include tenotomy (division of an overactive tendon), tendon transfer, arthrodesis (PIPJ) or toe
amputation.

Figure 34: Types of toe deformities. Source: 3 Point Products (2011).

81

Trauma

Trauma care may involve many different medical and surgical specialties including Accident &
Emergency, Orthopaedics, General Surgery, Vascular Surgery, Intensive Care & Anaesthesiology,
Neurosurgery, Urology, Cardiothoracic Surgery & Cardiology, Plastic Surgery and Maxillofacial
Surgery. In the UK, the specialty of orthopaedics is involved in the management of fractures,
dislocations, lacerations and penetrating injuries involving the upper and lower limbs. Where
there is a major vascular injury in a limb, vascular surgery or plastic surgery may be involved and
if there are concerns regarding skin / soft tissue coverage of a wound or peripheral nerve
division, plastic surgery are usually involved.

Orthopaedics is also involved in the rehabilitation of the trauma patient with limb injuries with
an essential input from physiotherapists and occupational therapists.

ManagementofMajorTrauma

With any high energy injuries (eg RTA, fall from height) the priorities are to save life and prevent
serious systemic complications ahead of preventing pain and loss of function from fractures or
dislocations.

Early death within the golden hour after injury from airway compromise, severe head injuries,
severe chest injuries, internal organ rupture and fractures associated with substantial blood loss
(pelvis, femur) can be avoided with rapid resuscitation and prompt, appropriate medical and
surgical care. Later deaths from MultiOrgan Dysfunction Syndrome and sepsis can also be
reduced with high quality early medical and surgical care.

The American College of Surgeons Committee on Trauma (ACS COT) have produced Advanced
Trauma Life Support (ATLS) guidelines which have been adopted worldwide and aim to
improve the quality of major trauma care and improve mortality from major trauma.

The principles of ATLS guidelines involve an initial primary survey where a quick assessment of
vital functions is made and appropriate management instigated followed by a secondary survey
involving a head to toe survey to detect other injuries of the head, face, chest, abdomen, pelvis,
genitourinary system, perineum, spine, neurological system and appendicular skeleton.
Primarysurvey

The primary survey consists of the ABCDE evaluation:

Airway management with cervical spine control
Breathing & ventilation
Circulation & bleeding control
Disability (neurological evaluation)
Exposure & environmental control
Airwaymanagementwithcervicalspinecontrol

Airway obstruction may be caused by foreign bodies, facial fractures, swelling from blunt trauma
or burns or reduced conscious level with loss of airway control. An obstructed airway will
prevent air inhalation and oxygenation of blood with rapid death if patency is not restored. Signs
of airway obstruction include noisy breathing, gurgling, stridor and agitation from hypoxia and
hypercapnoea. A patient who is able to speak has control of a clear airway.

A Glasgow Coma Score (GCS)of 8 or less implies loss of airway control and the first aid manoevre
of chinlift, jaw thrust corrects this. A definitive airway (cuffed endotracheal tube) is required
after this and an oropharyngeal (Guedel) airway or nasopharyngeal airway can provide
temporary control.

82


Any obstruction must be removed however if an obstruction cannot be removed expediently,
emergency cricothyroidotomy may be performed with a new airway created via a tube through
the cricothyroid membrane. Oxygenation and ventilation can be delivered through the new
airway.

When assessing and managing airway problems the Cspine should be protected by immobilizing
the head manually as movement with an undiagnosed Cspine injury could result in potentially
devastating spinal cord injury.
Breathingandventilation

All major trauma patients should receive high flow Oxygen via a tight fitting mask. Oxygenation is
best assessed with pulse oximetry.

An assessment of breathing is performed to diagnose life threatening tension pneumothorax,
open pneumothorax, flail chest, pulmonary contusion and massive haemothorax. Respiratory
distress, air hunger, tachypnea, tachycardia and cyanosis may be present.

Tension pneumothorax occurs when a puncture in the lung results in a one way valve between
the lung and pleural cavity resulting in accumulation of air around the lung which can result in
collapse and severe respiratory distress. The trachea may be palpably deviated to the opposite
side, respiratory distress will be apparent, tachycardia and hypotension will be present, neck
veins will be distended and there will be no air entry on the affected side. Emergency
management involved needle decompression with a large bore needle in the 2nd intercostal
space, midclavicular line before a chest drain is inserted.

Open pneumothorax may produce a sucking chest wound with air entering the pleural space
from outside during inspiration potentially resulting in tension pneumothorax. A chest drain
distant from the wound is inserted. Massive haemothorax can also compress the lung restricting
expansion. The affected hemithorax will be dull to percussion with reduced air entry. Again a
chest drain is required.

A flail chest occurs with segmental fractures of two or more ribs producing discontinuity of a
segment of the thoracic cage and paradoxical movement of that segment with reduced expansion
of the underlying lung. Assisted ventilation via a definitive airway is required. Pulmonary
contusion results in blood filling alveoli with reduction in ventilation. Assisted ventilation may be
required.
Circulation&haemorrhagecontrol

An initial assessment of adequacy of circulation and perfusion is performed by assessing the
patients pulse rate and volume as well as blood pressure. A cardiac monitor provides continuous
information to detect tachycardia, bradycardia and any arrhythmia. Bilateral large bore
peripheral venous access is achieved and all major trauma patients are given 2l of IV crystalloid
initially. Urinary catheterization and urine output monitoring are essential to guage fluid balance.
Minimum accepted urine output is 30ml/hour.

Hypovolaemic shock may occur due to internal (thoracic, abdominal, pelvis) or external
haemorrhage. Tachycardia is the first manifestation of hypovolaemia followed by reduction in
blood pressure. Confusion or lethargy may also be present.

Hypovolaemia should respond to fluid resuscitation. Transient response suggests ongoing
bleeding. No response with chest trauma, particularly penetrating injuries, may indicate cardiac
tamponade from haemorrhage within the pericardial sac (look for distended neck veins and
muffled heart sounds) which can be confirmed with an echocardiogram and may require needle
pericardiocentesis or surgery.

Exsanguinating haemothorax may need surgery (thoracotomy) to control.

83

Blunt or penetrating abdominal trauma may cause intraabdominal bleeding with perotonism on
examination. Suspicion of intraabdominal bleeding requires a surgical opinion and either an
emergency Ultrasound scan, CT scan of diagnostic peritoneal lavage (local anaethetic surgical
procedure with cathether placed in peritoneal cavity and warmed fluid instilled then drained to
detect blood). Intraabdominal bleeding requires emergency laparotomy to control bleeding and
repair or remove damaged organs.

Pelvic fractures can result in substantial blood loss from arterial bleeding (internal iliac artery &
branches), venous bleeding (pelvic venous plexus) and from fractured bone ends. In particular an
open book pelvic fracture (where the two hemipelvises are sprung apart) has a substantial risk
of like threatening haemorrhage and pelvic volume can be greatly increased with several litres of
blood loss before tamponade can occur. An open book pelvic fracture should be reduced as an
emergency with a pelvic binder or emergency external fixator to reduce the potential pelvic
volume and allow tamponade of bleeding to occur sooner.

Obvious external bleeding can be controlled by direct pressure with gauze (plug, press, elevate)
or with major peripheral arterial or venous bleeding a temporary tourniquet may be applied.
Disability
A quick neurologic assessment should be performed to establish the level of consciousness,
identify signs of severely raised intracranial pressure from intracranial haemorrrhage (pupil
fixed, dilated), identify signs of laterality of any intracranial injury and to determine the presence
and level of spinal cord injury (the most caudal level with preserved sensory and motor
function).

Level of consciousness is determined by the Glasgow Coma Score (Eye, Motor & Verbal
response). GCS of 8 or less implies severe head injury with potential loss of airway control and
requires placement of a definitive airway. Any history or signs of significant head injury (loss of
consciousness more than 5 minutes, >1 episode of vomiting, amnesia more than 30 minutes,
severe headache, obvious skull fracture, focal neurologic deficit, GCS < 15 at 2 hours after injury
or GCS <12 at any time) requires CT scanning to look for cerebral contusions or subdural /
extradural haematoma and neurological consultation should be sought. Elderly patients have a
higher risk of subdural haematoma and a lower threshold for CT scanning should be adopted.
Significant head injuries also increase the risk of Cspine injury and CT scanning of the cervical
spine should also be requested in the unconscious or confused patient.

Response to Assessment
Score
Best Motor Response
Obeys commands
6
Localizes pain
5
Normal withdrawal (flexion)
4
Abnormal withdrawal (flexion)decorticate 3
Extensiondecerebrate
2
None (flaccid)
1
Verbal Response
Oriented
5
Confused conversation
4
Inappropriate words
3
Incomprehensible sounds
2
None
1
Eye Opening
Spontaneous
4
To speech
3
To pain
2
None
1

84

Table 1: GCS, total score is based on the best motor response, the best verbal response and the
best eye opening . The best possible score is 15 whereas the worst possible score is 3. Refer to
neurology block for further information. Source: (Miller MD, 2012)


Along with head injury, alcohol and drugs can impair consciousness and cause patient
aggression. In major trauma, suspected head injury or where history is unreliable, aggressive
behavior or reduced coma score should not be assumed to be due to substance abuse and
observation or investigation for significant head injury is required.

Hypoxia and hypoperfusion can also lead to deterioration of conscious level and any sudden
reduction in GCS needs a quick reassessment of Airway, Breathing and Circulation.
Exposure

Adequate patient exposure should ensure that no major injuries are missed. The patient should
be kept warm to avoid hypothermia which can readily occur in the unconscious or immobile
patient. Warmed IV fluids should be administered.

Endofprimarysurvey

At the end of the primary survey a trauma series of Xrays (lateral Cspine, chest and pelvis x
rays) may be performed depending on the clinical condition along with Xrays of any other
significant musculoskeletal injuries (major long bone fractures).

The patient should be log rolled (a manoevre by 4 trained staff to avoid rotation of the spine and
inadvertent spinal cord injury if unstable spinal injury) and signs of spinal fracture (tenderness,
swelling) should be looked for and a PR examination performed (to detect PR bleeding and
assess anal tone & perianal sensation). The cervical spine may be cleared at this stage if the
patient is conscious, cooperative, not confused and has no clinical signs of cspine injury (no
tenderness, no pain on neck movements and no peripheral neurological deficit).

A urinary catheter should be passed (unless suspicion of urethral injury from pelvic injury call
urologist if blood at urethral meatus) and a nasogastric tube is usually passed to prevent
aspiration in the event of gastric dilatation which can occur in major trauma.

Formal ABGs give data regarding oxygenation, adequacy of ventilation and adequacy of perfusion
(acidosis). FBC, U&Es and Group & Save or Cross Match are sent. CT scans, Ultrasound or DPL
may be performed at this stage.
SecondarySurvey

The secondary survey should only proceed after the primary survey is completed and the patient
is stable. Any deterioration in the clinical condition requires a return to the start of the primary
survey. Some patients may never progress to the secondary survey and in some cases the
secondary survey may occur after lifesaving or stabilizing surgery.

The secondary survey is a headtotoe examination to detect other injuries (facial injuries,
lacerations, fractures, dislocations etc.). With high energy trauma, major injuries may be
distracting and more minor injuries may be missed on initial assessment and may not be
diagnosed until days after the event.

A more thorough history of the injury, past medical history and fasting status (in case of surgery)
is also obtained.
PolytraumaandDamageControlOrthopaedics

85

Polytrauma is where more than one major long bone is injured or where a major fracture is
associated with significant chest or abdominal trauma. With major trauma involving multiple
injuries, unstable major long bone fractures can cause ongoing blood loss with hypovolaemia,
pain, increased sympathetic response, amplification of the inflammatory response and fat
embolism which can result in deterioration of the patients clinical condition. Early stabilization
of major long bone fractures should be performed to optimize the patients condition and help
prevent Systemic Inflammatory Response Syndrome (SIRS), Acute Respiratory Distress
Syndrome (ARDS), MultiOrgan Dysfunction Syndrome (MODS) and death.

SIRS occurs when there is an amplification of inflammatory cascades in response to trauma with
pyrexia, tachycardia, tachypnea and leukocytosis. It is associated with a poorer prognosis.

ARDS may occur due to hypoperfusion, SIRS, aspiration or fat embolism with inflammation of the
lung parenchyma leading to inflammatory exudates forming in alveoli and impairment of gas
exchange. Positive pressure ventilation is required.

Hypovolaemia, SIRS and ARDS can lead to MODS and potential death. Older patients have less
physiologic reserves and are more prone to developing these serious complications.

In a case of polytrauma, rapid skeletal stabilization is required to limit the biological load of
trauma and to limit blood loss. This is known as Damage Control Orthopaedics with the aim of
preventing clinical deterioration by rapid skeletal stabilization. External fixators can be useful as
they can be rapidly applied with minimal blood loss. Intramedullary nails can be fairly rapidly
applied however there is an increased risk of fat embolism.

86

Thefractureprocessandfracturehealing

Fracture is the medical term for a break in the bone. Fractures can be due to direct trauma (eg
direct blow) however the majority are caused by indirect trauma (due to twisting or bending
forces). Fractures can be partial / incomplete (eg unicortical fracture from a stress fracture) or
complete. Fractures can also be classified as high energy (eg RTA, gunshot, blast, fall from height)
or low energy (eg trip, fall, sports injury). Very low injury fractures are usually due to an
underlying weakness of the bone resulting in a pathologic fracture.

Bone can heal (in a similar way to skin) by primary healing (1st intention) or secondary healing
(2nd intention). Primary bone healing occurs where there is minimal fracture gap (less than
about 1mm) and the bone simply bridges the gap with new bone from osteoblasts. This occurs in
the healing of hairline fractures and when fractures are fixed with compression screws and
plates. In the majority of fractures, there is a gap at the fracture site which needs to be filled
temporarily to act as a scaffold for new bone to be laid down. This is known as secondary bone
healing occurs.

Secondary cone healing involves an inflammatory response with recruitment of pluropotential
stem cells which differentiate into different cells during the healing process. The fracture process
of secondary bone healing is as follows:

Energy is delivered to the bone
Fracture occurs
Haematoma occurs with inflammation from damaged tissues
Macrophages and osteoclasts remove debris and resorb the bone ends
Granulation tissue forms from fibroblasts and new blood vessels
Chondroblasts form cartilage (soft callus)
Osteoblasts lay down bone matrix (collagen type 1) Enchondral ossification
Calcium mineralisation produces immature woven bone (hard callus)
Remodelling occurs with organization along lines of stress into lamellar bone

Figure 35: Secondary bone healing process. (inflammation soft callus hard callus
remodeling). Source: (Haspi Medical Anatomy & Physiology).


Soft callus is usually formed by the 2nd to 3rd week whilst hard callus takes approximately 612
weeks to appear. Secondary bone healing requires a good blood supply for oxygen, nutrients and
stem cells and also requires a little movement or stress (compression or tension). Lack of blood

87

supply, no movement (internal fixation with fracture gap), too big a fracture gap or tissue
trapped in the fracture gap may result in an atrophic nonunion. Smoking may severely impair
fracture healing due to vasospasm whilst vascular disease, chronic ill health and malnutrition
will also impair fracture healing. Hypertrophic non unions occur due to excessive movement at
the fracture site with abundant hard callus formation but too much movement give the fracture
no chance to bridge the gap.
Fracturepatterns

Five basic fracture patterns exist:

Transverse fractures occur with pure bending force where one side (convex side) fails in
compression and the other (concave) side fails in tension. Transverse fractures may not shorten
(unless completely displaced) but may angulate or result in rotational malalignment.

Oblique fractures occur with a shearing force (eg fall from height, deceleration). Oblique
fracture patterns have the benefit of being able to be fixed with an interfragmentary screw.
Oblique fractures tend to shorten and may also angulate.

Spiral fractures occur due to torsional forces. Again interfragmentary screws potentially can be
used. Spiral fractures are most unstable to rotational forces but can also angulate.

Comminuted fractures are fractures with 3 or more fragments. Comminution is generally a
reflection of a higher energy injury (or poor bone quality) and there may be substantial soft
tissue swelling and periosteal damage with reduced blood supply to the fracture site which may
impair healing. Comminuted fractures are very unstable and tend to be stabilized surgically.

A segmental fracture occurs when the bone is fractured in two separate places. These injuries
are very unstable and require stabilization with long rods or plates.

Figure 36:The five basic fracture patterns. Source: Luqmani R et al. (2013).

Describingafracture

A decision regarding the optimum management of a fracture depends on the site of the fracture,
whether its position is satisfactory or not and its stability (likelihood of displacing) which is
related to the fracture pattern and the degree of initial displacement.

A fracture of a long bone can be described according to the site of the bone involved in terms of
the proximal, middle or distal third. It can also be described according to the type of bone
involved diaphyseal (shaft), metaphyseal or epiphyseal.

88

A fracture at the end of a long bone (metaphyseal / epiphyseal) can be intraarticular (extending
into the joint) or extraarticular. Intraarticular fractures have a greater risk of stiffness, pain and
posttraumatic osteoarthritis, particularly if there is any residual displacement resulting in an
uneven articular surface.

The position of a fracture depends on the degree of displacement and angulation:

Displacement describes the direction of translation of the distal fragment and is described
using anatomic terms. Fractures can be described as anteriorly or posteriorly displaced and
medially or laterally displaced. In the forearm and hand anterior and posterior displacement are
typically substituted by volar (or palmar) and dorsal whilst medial and lateral displacement are
typically substituted by ulnar and radial (with respect to the anatomic position). Displacement
can be estimated with reference to the width of the bone (eg 25%, 50%, 75% displacement).
100% displacement is generally referred to as an offended fracture.

Figure 37: Medial displacement of the femur. Source: King MH (1987).

The degree of angulation describes the direction which the distal fragment points towards.
Angulation can be described as medial or lateral and anterior or posterior. In the upper limb
however, radial or ulnar and dorsal or volar angulation are typically used. In the lower limb
varus (distal fragment pointing towards the midline) and valgus (away from the midline) are
used instead of medial or lateral. Angulation can be measured in degrees from the longitudinal
axis of the diaphysis of a long bone.

Figure 38: Varus angulation of femur. Source: King MH (1987).

89

The displacement and angulation of a fracture gives information of the direction of forces
involved in the injury and gives information about the reversed direction of forces required to
reduce a fracture.

Residual displacement or angulation can lead to deformity, loss of function and abnormal
pressure on joints leading to posttraumatic OA.

Minor degrees of displacement and angulation may be acceptable depending on the bone
involved and the site of the fracture
Childrensfractures

Childrens fractures merit special attention for a number of reasons:

Childrens bones are more elastic and pliable and tend to buckle or partially fracture or splinter
with some degree of continuity of some fibres of bone (like breaking a green stick from a tree)
rather than break completely. Hence the terms buckle fracture and greenstick fracture.

Figure 39: Greenstick fracture. Source: Luqmani R et al. (2013).

The periosteum (which serves to increase the width/circumference of growing long bones) is
much thicker and tends to remain intact which can help stability and can assist reduction if
required.

Childrens fractures heal more quickly than adults due to the ticker periosteum which is a rich
source of osteoblasts. Children have much greater potential to remodel (change shape with bone
laid down along areas of stress according to Wolffs Law) as they grow with bone being formed
along the line of stress and children can correct angulation up to 10 per year of growth
remaining in that bone.

For these reasons childrens fractures tend to be surgically stabilized less frequently and greater
degrees of displacement or angulation can be accepted. If the fracture position is unaccepatable,
manipulation and casting may be all that is required accepting a degree of residual angulation or
displacement. Furthermore, if surgical stabilization is required for more unstable injuries, less
invasive temporary pins, wires and flexible rods tend to be used with plates and screws reserved
for very unstable periarticular injuries or where a fracture is associated with a dislocation and
loss of position may result in redislocation (eg Monteggia and Galeazzi injuries of the forearm).

Once a child has reached puberty (around 1214), fractures tend to be treated as an adults
fracture would as the remodeling potential is less.

Fractures around the physis (growth plate) also have the potential to disturb growth which could
result in a shortened limb or an angular deformity if one side of the physis is affected by growth
arrest.

90

SalterHarrisClassificationofPhysealFractures

Various patterns of physeal fractures exist with a classification linking patterns of injury to
prognosis. Prognosis is poorer as the classification progresses.

Figure 40: SalterHarris classification. Source: Miller MD (2012).

A SalterHarris I fracture is a pure physeal separation. This carries the best prognosis and is least
likely to result in growth arrest.

Most physeal fractures are SalterHarris II fractures. A SalterHarris II fracture is similar but has a
small metaphyseal fragment attached to the physis and epiphysis. Again the likelihood of growth
disturbance is low. SalterHarris II fractures are the commonest physeal farctures.

SalterHarris III and IV fractures are intraarticular and with the fracture splitting the physis,
there is greater potential for growth arrest. These fractures should be reduced and stabilized to
ensure a congruent articular surface and minimize growth disturbance.

A SalterHarris V injury is a compression injury to the physis with subsequent growth arrest.
These injuries cannot be diagnosed on initial xrays and are only detected once angular deformity
has occurred.
Nonaccidentalinjury(NAI)

Unfortunately the physical abuse of children occurs across society however child abuse occurs
more frequently in children living in poverty, in children with special needs or disability and in
children of parents who are substance abusers.

Multiple fractures of varying ages (with varying amounts of callus or healing) or multiple trips to
A&E with different injuries raises the suspicion of Non Accidental Injury or child abuse.

Other features which should raise suspicion include:

Inconsistent / changing history of events
Discrepancy of history between parents / carers
History not consistent with injury
Injuries not consistent with age of child eg non walking child
Multiple bruises of varying ages
Atypical injuries eg cigarette burns, genital injuries, torn frenulum, dental injuries, lower limb
and trunk burns
Rib fractures
Metaphyseal fractures in infants

Paediatricians should be involved early and any child considered at risk or under suspicion of
NAI should be admitted for safety and a full examination of the child and skilled history taking
from parents or carers should be performed by an experienced doctor.

91

Clinicalsignsofafracture

Clinical signs of a fracture include:

Localised bony (marked) tenderness not diffuse mild tenderness
Swelling
Deformity
Crepitus from bone ends grating with an unstable fracture

Not all musculoskeletal injuries require an Xray to exclude a fracture and in many injuries a
fracture can be excluded on clinical grounds avoiding unnecessary radiographs. Guidelines exist
for some injuries to assist with selecting which patients require Xray (eg Ottowa guidelines for
ankle injury). A useful rule is that if a patient cannot weight bear on an injured lower limb, Xray
of the painful area should be requested.
Investigationofafracture

Radiographs (xrays) are used to diagnose the majority of fractures with usually an AP and
lateral view required to assess the personality of the fracture. Some fractures may not be
obvious on one view but readily seen on the orthogonal (perpendicular) view hence two views
are always required. Oblique views can also be useful for complex shaped bones (eg scaphoid,
acetabulum, tibial plateau). However some fractures require further imaging for diagnosis or to
plan management.

XRAY trauma 280413 both bones forearm

A tomogram is a moving Xray to take images of complex bones. Their use is largely historic but
tomograms are still used to diagnose mandibular fractures.

CT (computerized tomography) can be used to assess fractures of complex bones (vertebrae,
pelvis, calcaneus, scapular glenoid) and can help determine the degree of articular damage and
help surgical planning for complex intraarticular fractures (eg. tibial plateau, distal tibia).

MRI can be used to detect occult fractures where there is clinical suspicion but a normal Xray (eg
hip, scaphoid).

Technetium bone scans can be useful to detect stress fractures (eg hip, femur, tibia, fibula, 2nd
metatarsal) as these may fail to show up on xray until hard callus begins to appear.
Complicationsoffractures

Early local complications of fractures include compartment syndrome, vascular injury with
ischaemia, nerve compression or injury, and skin necrosis.

Early systemic complications include hypovolaemia, fat embolism, shock, Acute Respiratory
Distress Syndrome, acute renal failure, Systemic Inflammatory Response Syndrome, MultiOrgan
Dysfunction Syndrome and death.

Late local complications include stiffness, loss of function, Chronic Regional Pain Syndrome,
infection, nonunion, malunion, Volkmanns ischaemic contracture, post traumatic osteoarthritis
and deep vein thrombosis.

The main late systemic complication of fractures is pulmonary embolism which tends to occur
several days to weeks after injury but can occur much sooner (occasionally within a day).
Compartmentsyndrome

Compartment syndrome is a serious complication and surgical emergency. Groups of muscles are
bound in tight fascial compartments with limited capacity for swelling. With bleeding and

92

inflammatory exudate from fracture and injury, pressure begins to rise. Rising pressure can
compress the venous system resulting in congestion within the muscle and secondary ischaemia
as oxygenated arterial blood cannot supply the congested muscle. Muscle ischaemia is
manifested by severe pain and pressure rises can also compress nerves resulting in
paraesthesiae and sensory loss. The cardinal clinical sign is increased pain on passive stretching
of the involved muscle. The limb will be tensely swollen and the muscle is usually tender to
touch. Loss of pulses is a feature of end stage ischaemia and the diagnosis has been made too late.
Once compartment syndrome has been clinically suspected, removal of any tight bandages may
cause temporary relief and emergency fasciotomies involving incisions through skin and fascia to
relieve constriction should be performed. The open wound are left for a few days before
secondary closure however many wounds require split skin grafting. If left untreated ischaemic
muscle will necrose resulting in fibrotic contracture known as Volkmanns ischaemic contracture
and poor function.

Figure 41: Fasciotomy on the medial wound (A). Fasciotomy on the lateral wound, present of
necrotic muscle (B). Source: Muchow RD et al. (2010).

Nerveinjury

Nerve injury associated with a fracture is usually a neurapraxia or axonotmesis.

A neurapraxia occurs when the nerve has a temporary conduction defect from compression or
stretch and resolve over time with full recovery (can take up to 28 days).

Axonotmesis occurs from either a sustained compression or stretch or from a higher degree of
force. Although the nerve remains in continuity and the internal structure (endoneurial tubes)
remain intact, the long nerve cell axons distal to the point of injury die in a process known as
Wallerian degeneration. The axons then regenerate along the endoneurial tubes at a rate of 1mm
per day. Longer peripheral nerves therefore take longer to recover. Recovery is variable and full
power or sensation may not be achieved. Recovery can be predicted by nerve conduction studies
from around a month from the time of injury.

93


A neurotmesis is a complete transection of a nerve and is rare in closed injuries but can occur in
penetrating injuries. No recovery will occur unless the affected nerve is surgically repaired. Again
recovery is variable.

The majority of nerve injuries associated with a fracture (or dislocation) usually resolve or
improve with time. The presence of a nerve injury is not an indication for surgical exploration
unless there is evidence of nerve entrapment within the fracture causing severe neuralgic pain. If
a nerve injury occurs after fracture manipulation it can be assumed that the nerve is trapped in
the fracture site. With most fracture related nerve injuries, observation for recovery is all that is
required.

If recovery from an axonotmesis or neurotmesis is poor, nerve grafting using an expendable
cutaneous nerve can help and tendon transfers to recruit muscles with intact nerve supply and
alter their mechanics by changing their insertion can improve function.

Some injuries are characteristically associated with particular nerve injuries:

Colles fracture and acute median nerve compression / carpal tunnel syndrome
Anterior dislocation of the shoulder and axillary nerve palsy
Humeral shaft fracture and radial nerve palsy (in spiral groove)
Supracondylar fracture of the elbow and median nerve injury (usually anterior
interosseous branch)
Posterior dislocation of the hip and sciatic nerve injury
Bumper injury to lateral knee and common peroneal nerve palsy

Vascularinjury

Vascular injury can happen with penetrating and blunt trauma. Vessels can be stretched,
compressed, torn or transected. Partial tears affecting the arterial intima can thrombose
resulting in arterial occlusion.

Whilst vascular injuries are uncommon in trauma, the consequences can be significant. Distal
limb ischaemia risks subsequent amputation. Haemorrhage from arterial or venous injury may
result in hypovolaemic shock. Certain injuries have a higher risk of concomitant vascular injury.
Penetrating injuries can result in transection of a vessel. Knee dislocation risks popliteal artery
injury, paediatric supracondylar fracture of the elbow risks brachial artery injury whilst shoulder
trauma can result in axillary artery compromise. Pelvic fractures can be associated with life
threatening haemorrhage from arterial or venous bleeding.

Any signs of reduced distal circulation (reduced or absent pulses, pallor, delayed capillary refill,
cold to touch) mandates urgent vascular surgery review and emergency surgical management.
Urgent angiography in theatre may help localize the site of arterial occlusion. Temporary
restoration of circulation can be achieved with use of a vascular shunt or vascular repair with
either a bypass graft or endoluminal stent can be perfomed. Skeletal stabilization with internal or
external fixation should be performed to protect the repair from shearing force.

Ongoing haemorrhage from arterial injury in the pelvis can be controlled by angiographic
embolization performed by interventional radiologists.
Openfractures

The skin acts as a vital barrier to bacteria however once breached bacteria (including normal
skin bacterial flora) can enter a wound and cause infection.

Open fractures can either occur due to a spike of fractured bone from within puncturing the skin
(so called inside out injury) or due to laceration of the skin from tearing or penetrating injury
(so called outsidein injury). Open fractures should be managed expediently to prevent

94

infection at the fracture site which might result in nonunion and is very difficult to eradicate.
Bone infection after open fracture of a long bone often requires extensive removal of bone with
shortening which may require complex surgery to lengthen the bone. Some infected nonunions
ultimately lead to amputation.

The higher the energy of the injury, the amount of contamination, any delay in appropriate
treatment and problems with wound closure increases the risk of infection. The presence of a
concomitant vascular injury raises the risk of amputation. A classification system (the Gustilo
classification) exists to describe the degree of contamination, the size of the wound, whether the
wound will be able to be closed or require plastic surgery cover and the presence of an
associated vascular injury.

Initial management in the Accident & Emergency department includes IV broad spectrum
antibiotics typically Flucloxacillin to cover gram positive organisms, Gentamicin to cover gram
negatives and Metronidazole to cover anaerobes if there is soil contamination. A sterile or
antiseptic soaked dressing should be applied to the wound to prevent further contamination
before the fracture is splinted.

In general, open fractures require fairly prompt surgery (as soon as possible or first on the next
day trauma list if during the night). Surgical management involves removal of all contamination
and excision of nonviable soft tissue, known as debridement. Dead or devitalized tissue may
serve to harbor infection with the immune system unable to access the devascularised tissues.
Additionally an unstable fracture may produce haematoma which acts as a culture medium for
bacteria and may cause additional necrosis. Open fractures are also often higher energy and
delayed union is more common. Furthermore open fractures are also difficult to treat in plaster
cast as frequent wound inspections are required. For all these reasons, open fractures are
usually stabilized with internal or external fixation providing an early and thorough
debridement is performed.

If the wound is not grossly contaminated and all remaining skin and muscle is viable, if the
wound can be closed without undue tension on the skin edges, the wound can be closed
primarily. Any wound tension may result in skin necrosis and wound breakdown. Any wound
which cannot be closed primary requires either skin grafting (usually split thickness skin
grafting, SSG), local flap coverage or even free flap coverage from plastic surgery. Tissues which
readily accept a skin graft include muscle, fascia and granulation tissue. Paratenon and
periosteum can also accept a skin graft. A skin graft will not take on bare tendon, bone or any
exposed metalwork. Skin grafts also may not take on fat due to poor vascularization.

If there is any doubt over viability of soft tissues or if the wound is heavily contaminated, it is
usually safer to leave the wound open to allow ongoing infection to drain out and to return to
theatre for further debridement in 48 hours as necrotic tissue will have declared itself by this
time. The wound may be closed secondarily or plastic surgical flap coverage and/or skin grafting
may be required.
Skinandsofttissueproblems

With higher energy injuries or with fragile skin (eg. due to age, steroids, rheumatoid arthritis) an
injury may jeopardise the viability of the overlying skin. A protruding spike of bone or tension on
the skin from deformity can lead to devitalisation and necrosis with skin breakdown. In the
situation where a fracture is causing excessive pressure on skin, as manifested by tenting of the
skin and blanching, the fracture should be reduced as an emergency (under analgesia +/
sedation) to avoid subsequent necrosis.

A shearing force on the skin can result in avulsion of the skin from its underlying blood vessels
known as degloving which can result in skin ischaemia and necrosis. The skin will not blanch
on pressure and may be insensate. Underlying haematoma may also increase pressure on the
skin occluding capillaries. The degloved area may take a few days to declare itself (demarcate)
and may require skin grafting or flap coverage.

95

The amount of soft tissue swelling and bruising (contusion) is usually a reflection of the energy of
the injury involved. Fracture blisters can occur due to inflammatory exudates causing lifting of
the epidermis of the skin (much like a burn). A surgical wound through swollen and contused
skin and soft tissues is not advisable as the wound may not be able to be closed (leaving a route
for subsequent infection) or excessive tension on the wound may lead to necrosis and wound
breakdown. The management of the soft tissues is fundamental to the management of any
underlying fracture and indirect methods of stabilization (see later) may be appropriate.

Figure 42: Due to excessive soft tissue swelling and contusions, external fixators are more
appropriate than internal fixators in high energy tibia plateau fracture. Source: Luqmani R et al.
(2013).
Mangledextremity

The more severe the injury, the greater the chance of necrosis and/or poor function. In the case
of mangled extremity from extensive bone and soft tissue damage (eg crushing), poorer
outcomes occur in higher energy injuries, injuries associated with prolonged ischemia and/or
neurological injury, injuries occurring with hypovolaemic shock and increasing age of the patient.
In certain cases of mangled extremity, it may be wiser to perform early amputation to produce a
more functional outcome and avoid multiple surgeries with which a poor result can be predicted.
DVT

Deep vein thrombosis can occur particularly after pelvic or major lower limb fractures with a
period of immobility. Prophylaxis should be given (usually LMWH) to all atrisk patients.
Suspected DVT requires duplex scanning and anticoagulation.
Fracturedisease

Fracture disease is a term used to describe stiffness and weakness due to the fracture and
subsequent splintage in cast. Most cases resolve with time and may be helped with
physiotherapy.
Delayedunion

Different fractures heal at different rates whilst healing is also dependent on the energy of the
injury (comminution, soft tissue damage) as well as the age of the patient and health status.

The tibia is one of the slowest healing bones in the body with fractures typically taking around16
weeks and sometimes over a year to unite. Femoral shaft fractures also typically take 34 months
to heal. Metaphyseal fractures tend to heal more quickly than cortical fractures.

96


A delayed union is a fracture that has not healed within the expected time. Infection can result in
a delayed union and if infection is diagnosed, healing can occur if the infection is suppressed with
antibiotics however the fracture may go on to an infected nonunion.
Nonunion

As previously described hypertrophic nonunion can occur due to instability and excessive
motion at the fracture site whilst atrophic nonunion can occur due to rigid fixation with a
fracture gap, lack of blood supply to the fracture site, chronic disease or soft tissue interposition.
Infection can also lead to atrophic or hypertrophic nonunion.

Some fractures are particularly prone to problems with healing due to poor blood supply
including scaphoid waist fractures, fractures of the distal clavicle, subtrochanteric fractures of
the femur and a Jones fracture of the fifth metatarsal. Some intraarticular fractures may not
unite due synovial fluid inhibiting healing if a fracture gap exists (intracapsular hip fracture,
scaphoid fracture).

Any fracture stabilization is a race between bone healing and implant failure as ultimately all
implants including plates and intramedullary nails will break due to fatigue failure. Approximate
reduction of the fracture permits quicker healing and allows the bone to share the load earlier
however apposition of bone ends may not be possible in comminuted fractures and higher
energy injuries may have disruption of the local blood supply.

Hypertrophic nonunions are due to instability and often the application of a plate is sufficient to
ensure subsequent union of the fracture.

Atrophic nonunions typically require the removal of fibrous tissue at the fracture site,
restoration of bleeding bone ends, restoration of medullary canal continuity, bone grafting to
stimulate bone formation and to act as a scaffold for new bone to grow into and internal or
external fixation with compression across the fracture.

In any nonunion, evidence of infection should be sought (by CRP and bacteriological sampling).
If infection is diagnosed, surgical removal of dead and infected bone is required often with
shortening of the bone. Special circular frame external fixators may be used with the advantages
of applying compression at the fracture site, the ability to adjust alignment and the ability to
lengthen the shortened bone.

Infectedfracturefixation

Fractures can still unite if the infection is suppressed and for acute infections antibiotic therapy
with or without surgical washout may be adequate. For infections present for longer than a few
weeks, fracture healing may still be accomplished with antibiotic suppression but the metalwork
will need later removal. If the infection cannot be suppressed and becomes too problematic
(sepsis, discharging sinus), surgery is required with removal of all implants and debridement of
infected bone.

Depending on the scenario, different strategies can be used. For medullary infection from an
infected intramedullary nail, the medullary canal can be reamed out (cored out with a flexible
drill) and a new nail implanted. Alternatively, an external fixator can be applied to give stability
with the advantage of some systems of being able to compress the bone ends and gradually
lengthen the bone if it has been substantially shortened. This would also be appropriate for
infected nonunion of a plate and screw fixation.

Malunion

97

Malunions can cause cosmetic deformity, interfere with function and result in abnormal
pressure on adjacent joints risking posttraumatic OA.

Some deformities are particularly poorly tolerated (eg internal rotation of the tibia leads to
awkward gait, volar angulation of the distal radius leads to very poor grip strength). Malunited
Colles fractures can result in weakness, stiffness and chronic pain.

Significant malunion can be corrected by osteotomy and acute correction held with a plate &
screws or with a circular external fixator (which can be adjusted as necessary).
AVN

Fractures of the femoral neck, scaphoid and talus are prone to developing AVN. Not all cases of
AVN are symptomatic but many cases require surgical management in the form of THR for the
hip or arthrodesis of the wrist or ankle for the scaphoid and talus respectively.
PosttraumaticOA

Post traumatic OA can occur due to intraarticular fracture, ligamentous instability or fracture
malunion. Its treatment may involve analgesia, bracing / splinting, arthrodesis or joint
replacement.
ComplexRegionalPainSyndrome(CRPS)

CRPS (formerly known as Regional Sympathetic Dystrophy, Sudecks atrophy and algodystrophy)
is a poorly understood heightened chronic pain response after injury. Charcteristics are variable
but include constant burning or throbbing, sensitivity to stimuli not normally painful (allodynia)
including cold or light touch, chronic swelling, stiffness, painful movement and skin colour
changes. It can be caused by a peripheral nerve injury (type 2) but often is not (type 1).

Management is difficult and requires specialist pain services. Pharmacological agents including
analgesics, antidepressants (amitriptyline), anticonvulsants (gabapentin) and steroids may help.
TENS machines, physiotherapy, lidocaine patches and sympathetic nerve blocking injections may
also help.
Systemiccomplicationsoffractures

Hypovolaemia, Fat embolism, ARDS, SIRS and MODS have been discussed earlier. The principal
late systemic complication particularly after pelvic of lower limb fracture is pulmonary
embolism.
Assessmentofaninjuredlimb

The assessment of an injured limb should include assessment of whether the injury is open or
closed, an assessment of the distal neurovascular status (pulses, capillary refill, temperature,
colour, sensation, motor power), whether there is a compartment syndrome present and an
assessment of the status of the skin and soft tissue envelope.
Initialmanagementofalongbonefracture

Initial fracture management involves clinical assessment of the injured limb as above, analgesia
(usually iv morphine), splintage / immobilization of the limb and investigation (usually Xrays).

Splintage or immobilization may involve the application of a temporary plaster slab (known as a
backslab), a sling, an orthosis or a Thomas splint (for femoral shaft fractures).

If a fracture is obviously grossly displaced, if there is an obvious fracture dislocation (eg of the
ankle) or if there is risk of skin damage from excessive pressure, reduction of the fracture should
be performed before waiting for xrays. Xrays post reduction should still demonstrate any
fractures adequately.

98

Definitivefracturemanagement

Definitive management of a fracture depends on which bone is broken, the location of the
fracture on the bone, the fracture pattern, the position of the fracture (displacement, angulation),
the stability of the fracture, whether it is open or closed, the presence of associated injuries, the
neurovascular status, the status of the soft tissue envelope, the age of the patient, the functional
status of the patient and the presence of any significant comorbidities.

In general terms undisplaced, minimally displaced and minimally angulated fractures which are
considered to be stable are usually treated nonoperatively with a period of splintage or
immobilization and then rehabilitation.

Displaced or angulated fractures where the position is deemed unacceptable require reduction
under anaesthetic (GA, spinal, peripheral nerve block, Biers block). Closed reduction and cast
application may be performed with serial xrays to ensure no loss of position. Unstable injuries
may be treated with surgical stabilisation which may involve the use of small percutaneous pins
(Kwires) for small fragments, cerclage wires, screws, plates & screws, intramedullary nails or
external fixation.

Unstable extraarticular diaphyseal fractures can be fixed with Open reduction and Internal
Fixation (ORIF) using plates and screws with the aim of anatomic reduction and rigid fixation
leading to primary bone healing. It may be preferable in some fractures to avoid ORIF
particularly where the soft tissues are too swollen, where the blood supply to the fracture site is
tenuous (high energy), where ORIF may cause extensive blood loss (eg femoral shaft) or plate
fixation may be prominent (eg tibia). In this case closed reduction and indirect internal fixation
with an intramedullary nail with dissection distant to the fracture site may be used with the aim
of a functional reduction and stable fixation allowing micromotion required for secondary bone
healing. Another alternative for extraarticular diaphyseal fractures is external fixation which
again aims for secondary bone healing however carries the risk of pin site infection and
loosening.

Displaced intraarticular fractures require anatomic reduction and rigid fixation by way of ORIF
using wires, screws and plates. Fractures involving a joint with predictable poor outcome may be
treated with joint replacement or arthrodesis.

The management of open fractures, associated neurovascular injury and compartment syndrome
have been previously discussed.

Elderly patients with comorbidites, osteoporosis and dementia are at higher risk of
complications of surgery, failure of fixation and failure to rehabilitate satisfactorily. Elderly
patients also tend not to have as high a functional demand and therefore older patients may be
more likely to be treated nonoperatively. Of course thorough discussion of the risks and
potential benefits of any surgery should occur with the patient or their relatives.
Signsoffracturehealingandnonunion

Not all fractures need to have radiographic evidence of fracture union. Many fractures,
particularly extraarticular cancellous bone fractures are predictably expected to heal and do not
routinely need followup xrays. For many evidence of healing is determined by clinical
assessment. Symptoms and signs of fracture healing include:

Resolution of pain and function
Absence of point tenderness
No local oedema
Resolution of movement at fracture site

Conversely, clinical signs of nonunion include:

Ongoing pain

99

Ongoing oedema
Movement at the fracture site

Bridging callus may be seen on Xray however in cases where doubt exists over bony union, CT
scans may confirm or exclude bridging callus.

Dislocations&Instability

Any dislocation should be reduced as soon as possible. Most dislocations can be reduced by
closed manipulation under sedation and analgesia or occasionally general or regional
anaesthetic. Delayed presentation of a dislocation (eg in alcoholics) increases the risk of
requiring an open reduction and recurrent insatbility.

Dislocations may occur after significant trauma however people with hypermobility (including
Ehlers Danlos and Marfans) may sustain a dislocation with a seemingly innocuous injury and
some can voluntarily dislocate joints (eg shoulder).

Dislocations can occur with associated injuries including tendon tears, nerve injury, vascular
injury and compartment syndrome. Recurrent dislocation may require soft tissue repair /
reconstruction or occasionally bony surgical prcedures.

Fractures can occur with dislocations (known as fracturedislocation) and these may reduce with
closed reduction however ORIF may be required if reduction cannot be achieved, if a bony
fracgment prevents congruent reduction or if the joint is very unstable.

Softtissueinjury

Ligaments and tendons can be sprained (intrasubstance tearing of some fibres), partially torn or
completely ruptured. Muscle tears can also occur with rapid resisted contraction.

Ligament ruptures can be graded as grade I (sprain), grade 2 (partial tear) and grade 3 (complete
tear).

Figure 43: Grade of ligament injury: sprain (a), partial tear (b), complete tear (c). Source: Dandy
D and Edwards DJ (2009)


The mainstay of treatment for most soft tissue injuries is RICE Rest, Ice, Compression,
Elevation to reduce initial swelling followed by early movement to prevent stiffness.

100

Some complete ligament ruptures result in joint instability and may need repair, tightening
(advancement) or graft reconstruction.

Complete tears of tendons fundamental for function (quadriceps tendon, patellar tendon,)
require surgical repair for restoration of function. Some complete tendon tears can be treated
conservatively (Achilles tendon, rotator cuff, long head of biceps brachii, distal biceps) however
repair may be warranted to restore function.

Figure 44: Patient with ruptured biceps tendon, which can be painful and disabling. Source:
Dandy D and Edwards DJ (2009).


Tendons may also be divided with penetrating incised wounds. Flexor and extensor tendon
injuries in the hand and wrist are particularly common and usually require surgical repair.

101

RegionalTrauma
Spine
Cspinefractures

Cspine fractures are commonly high energy injuries (RTA, fall from height) and may be
associated with head injury. Potentially dangerous unstable fractures may be missed in the
unconscious or confused patient which may result in spinal cord injury. One should have a low
threshold for Cspine immobilization with a hard collar and sand bags or blocks on a spinal board
in any high energy injury or head injury (ABCD Airway with Cspine control).

The Cspine can be cleared in a conscious and cooperative patient through clinical assessment.
Lack of midline tenderness, no pain on gentle head movement and no evidence of neurologic
injury obviates the need for further investigation and the cspine can be cleared. If there is any
doubt imaging in the form of XRays (AP & lateral views +/ odontoid peg open mouth view if
upper cspine symptoms / signs) or CT of the cspine is required.

Any suspected Cspine injury requires a full trauma assessment (ABCD) and a full neurological
examination including peripheral motor function & coarse touch sensation, upper & lower limb
reflexes, cranial nerve evaluation, rectal examination and assessment of bulbocavernous reflex.

High cspine fractures or dislocations may be fatal especially if above C3 (above phrenic nerve
C3,4,5).

More stable cspine injuries can be treated in a firm cervical collar. Unstable injuries may require
immobilization in a halo vest which is a type of external fixator with 4 pins into the skull. Some
unstable injuries require surgical stabilization including fusions, wiring or internal fixation.
Subluxations and dislocations may require traction for reduction and halo application or
operative stabilization whilst burst fractures with neurologic deficits may require traction to
decompress the spinal canal.

Figure 45: A Halo vest. Source: 3tailer ().

Thoracolumbarspinefractures

The majority of thoracolumbar spine fractures occur due to motor vehicle accidents or falls from
a height. In the elderly with osteoporosis osteoporotic wedge insufficiency fractures can occur
which usually do not require anything other than symptomatic treatment.

102


Any high energy thoracolumbar injury requires full trauma evaluation and neurological
assessment. 1520% of thoracolumbar fractures have an associated neurological deficit.

Whilst osteoporotic low energy fractures tend to be compression / wedge fractures which are
relatively stable, younger patients with higher energy injuries tend to have burst fractures with
involvement of the posterior elements or Chance flexiondistraction fractures with failure of
the posterior ligaments which may be unstable and may require operative stabilization. More
stable injuries (without substantial displacement or collapse) of the thoracic spine may be
treated with a brace to limit flexion and prevent kyphosis whilst more stable lumbar injuries may
be treated with a plaster jacket to preserve the lumbar lordosis. Posterior bony or ligamentous
involvement may be detected as localized tendeness, swelling or a palpable defect on
examination.

Indications for surgery include:

Presence of neurological deficit especially if progressive or very unstable injury
Unstable injury pattern with substantial loss of vertebral height, displacement or
involvement of the posterior ligamentous structures.

Surgery may involve stabilization with pedicle screws and rods, spinal fusion and decompression
(creation of space around the cord or nerve roots) in the presence of a neurologic deficit.
Spinalcordinjury

The spinal cord or nerve roots can be damaged from contusion, compression, stretch or
laceration. Vascular disruption and oedema may result in further ischaemic damage and
hypotension, hypoxia and inflammatory responses may also result in secondary damage.

Spinal shock is a physiologic response to injury with complete loss of sensation and motor
function and loss of reflexes below the level of the injury. Spinal shock usually resolves in 24
hours with return of reflexes and the severity of a spinal cord injury may not be determined until
after spinal shock has resolved. The bulbocavernous reflex is a reflex contraction of the anal
sphincter with either a squeeze of the glans penis, tapping the mons pubis or pulling on a
urethral catheter. The bulbocavernous reflex is absent in spinal shock and its return signals the
end of spinal shock.

Neurogenic shock occurs secondary to temporary shutdown of sympathetic outflow from the
cord from T1 to L2, usually due to injury in the cervical or upper thoracic cord leading to
hypotension and bradycardia which usually resolves within 2448 hours. Priapism from
unopposed parasympathetic stimulation may be present. Neurogenic shock is treated with IV
fluid therapy. Neurogenic shock must be differentiated from other forms of shock (hypovolaemic
shock is much more common in trauma cases and should respond to fluid replacement therapy).

Spinal cord injuries can be classified as complete or incomplete. Complete spinal cord injury
results in no sensory or voluntary motor function below the level of the injury (reflexes should
return). The level of the injury is determined by the most distal spinal level with partial function
(after spinal shock has resolved) as determined by the presence of dermatomal sensation and
myotomal skeletal muscle voluntary contraction. The prognosis for recovery from complete cord
injuries is poor.

103

Figure 46: Dermatome of upper limb (a) and lower limb (b). Source: Dandy D and Edwards DJ
(2009).

Figure 47: Myotomes of upper limb. Source: Luqmani R et al. (2013).

104


Figure 48: Myotomes of upper limb. Source: Luqmani R et al. (2013).


Picture dermatomes & table myotomes.

With incomplete injuries, some neurologic function (sensory and/or motor) is present distal to
the level of injury. In general, the greater the function present, the faster the recovery is and the
better the prognosis. Sacral sparing with preservation of perianal sensation, voluntary anal
sphincter contraction and big toe flexion (FHL muscle, S1/2) indicates some continuity of the
corticospinal (motor) and spinothalamic (course touch, pain, temperature) tracts. The presence
of sacral sparing indicates an incomplete cord injury with a better prognosis than a complete
injury.

Different syndromes / patterns of injury exist depending on the area of the cord injured:

Central cord syndrome is the most common injury pattern and usually occurs with a
hyperextension injury in a cervical spine with osteoarthritits. Often there is no associated
fracture or dislocation (Spinal Cord Injury Without Radiographic Abnormality, SCIWORA).
Paralysis of the arms more than the legs occurs due to the corticospinal (motor) tracts of the
upper limbs being more central and those for the lower limbs being more peripheral in the cord.
Sacral sparing is typically present. (Diagram)

105

Figure 49: Central cord syndrome. Source: Sinaiem ().

Anterior cord syndrome results in loss of motor function (corticospinal tracts) as well as loss of
coarse touch, pain and temperature sensation (lateral spinothalamic tract) whilst proprioception,
vibration sense and light touch are preserved (dorsal columns).

Figure 50: Anterior cord syndrome. Source: Sinaiem ().

Posterior cord syndrome with loss of dorsal column function is rare.

BrownSequard syndrome results from hemisection of the cord usually from penetrating injury
eg stab wound. Ipsilateral paralysis and loss of dorsal column sensation occurs with contralateral
loss of pain, temperature and coarse touch sensation. This is due to nerve fibres of the
spinothalamic tracts crossing to the other side of the cord one or two levels above their entry
into the cord whilst the nerve fibres of the other tracts cross higher up in the medulla.

106

Figure 51: BrownSequard syndrome. Source: Sinaiem ().

Spinal cord injuries are often high energy injuries and often occur with other injuries. Full ATLS
primary survey with resuscitation and protection of the cervical and thoracolumbar spine is
mandatory. Shock (organ hypoperfusion) in the presence of spinal injury should not be assumed
to be neurogenic and hypovolaemic shock is much more common. Adequate resucitation
prevents secondary hypoxic cord damage.

Treatment of spinal cord injury is aimed at preventing further damage and preventing
complications of paralysis. Appropriate immobilization (cervical collar & sandbags, spinal board)
helps prevent further damage where an unstable fracture or dislocation exists. Early IV steroid
(methylprednisolone) administration can lead to slight improvement due to decreased
inflammation around the cord. Traction may be required to reduce dislocations or stabilize
unstable cervical spine injuries. Surgery may be required to relieve pressure on the cord or to
stabilize unstable injuries. Strict attention to pressure areas with special spinal beds helps
prevent pressure sores from paralysis. Ventilatory support may be required for loss of
intercostal muscle function (T1T12). A multidiscliplinary approach with involvement of
specialist nurses, neurosurgeons, spinal injury physicians, orthopaedic surgeons,
physiotherapists, occupational therapists, psychologists and social services is typically required
for treatment and rehabilitation.
Pelvis

Pelvic fractures in younger patients occur due to high energy. Older patients with osteoporosis
can sustain pubic rami fractures from low energy injuries. The pelvic ring is formed by the
sacrum, ilium, ischium and pubic bones with strong supporting ligaments. If the pelvic ring is
disrupted in one place, there is invariably a further disruption (either fracture or ligamentous
injury at the SI joint) elsewhere in the ring (like a polo mint it, you cant break it in only one
place). Branches of the internal iliac arterial system and the presacral venous plexus are prone
to injury with risk of serious hypovolaemia. Nerve roots and branches of the lumbosacral plexus
are prone to injury.

3 general patterns of injury exist:

107

A lateral compression fracture occurs with a side impact (eg RTA) where one half of the pelvis
(hemipelvis) is displaced medially. Fractures through the pubic rami or ischium are accompanied
by a sacral compression fracture or SI joint disruption.

A vertical shear fracture occurs due to axial force on one hemipelvis (eg fall from height, rapid
deceleration) where the affected hemipelvis is displaced superiorly. The sacral nerve roots and
lumbosacral plexus are at high risk of injury and major haemorrhage may occur. The leg on the
affected side will appear shorter.

An anteroposterior compression injury may result in wide disruption of the pubic symphysis
the pelvis opening up like the pages of a book the socalled open book pelvic fracture.
Substantial bleeding from torn vessels occurs and as the pelvic volume increases exponentially
with the degree of displacement, with widely displaced injuries the pelvis can contain several
litres of blood (ie the entire circulating volume) before tamponade and clotting will occur.

Figure 52: YoungBurgess Classification of pelvis fracture. Source: Miller MD (2012)

Due to the high energy typically involved, pelvic fractures are usually associated with other
injuries and require prompt assessment and resuscitation. Blood loss is treated with fluids or
blood. With open book pelvic fractures it is critical to promptly reduced the displacement and
minimizing the pelvic volume to allow tamponade of bleeding to occur. Manual manipulation and
application of a tied sheet or a special pelvic binder will hold the reduction temporarily whilst an
external fixator will provide more secure initial stabilization. With a vertical shear fracture, the
application of skin traction may give some stability and limit further bleeding. Ongoing

108

haemodynamic instability despite these measures may require angiogram and embolization or
open packing of the pelvis if laparotomy is required for coexisting intraabdominal injuries.

Bladder and urethral injuries (blood at the urethral meatus) may also occur and urinary
catheterization may risk further injury. Urological assessment and intervention may be required.
A PR exam is mandatory to assess sacral nerve root function and to look for the presence of
blood. The presence of blood indicates a rectal tear rendering the injury an open fracture and
carries a higher risk of mortality. General surgical review is mandatory and defunctioning
colostomy may be required.

In general terms, minimally displaced pelvic fractures are stable and are treated conservatively
with protected weight bearing for a couple of months. Substantially displaced injuries have a
greater risk of chronic pain and poor function and are usually treated with ORIF. CT scanning is
required to evaluate the location of fractures and the degree of displacement.

Low energy pubic rami fractures in the elderly tend to be minimally displaced lateral
compression injuries (with sacral fracture or SI joint disruption posteriorly) and settle with
conservative management over time.
Acetabularfractures

Acetabular fractures are usually high energy injuries in the younger patient but can be low
energy in the older patient. Posterior wall fractures may be associated with a hip dislocation.

The pattern of the fracture can be difficult to determine on plain Xrays (oblique views may help)
and CT scans help to determine the pattern of the fracture and are essential for surgical planning.

Undisplaced fractures or small wall fractures may be treated conservatively. As with most intra
articular fractures, unstable or displaced fractures require anatomic reduction and rigid fixation
in the younger patient to reduce the risk of post traumatic OA. Older patients may be treated with
total hip replacement either early (with an uncemented cup and screws) or delayed.
Shoulder
Proximalhumerusfracture

Proximal humerus fractures are common with the majority being low energy injuries in
osteoprotic bone due to a fall onto the outstretched hand or directly onto the shoulder.

The most common pattern is a fracture of the surgical neck (rather than the anatomic neck) with
medial displacement of the humeral shaft due to pull of the pectoralis major muscle. The greater
and lesser tuberosities may also be avulsed with the attachments of Supraspinatus, Infraspinatus
and teres minor for the greater tuberosity and subscapularis for the lesser tuberosity. Isolated
fractures of the greater tuberosity and headsplitting intraarticular fractures can also occur.

Many minimally displaced proximal humerus fractures are treated conservatively with a sling
and gradual return to mobilization. With displaced fractures, the position often improves once
muscle spasm settles. Persistently displaced fractures are usually treated with internal fixation
(plate, screws, wires or intramedullary nail) but stiffness, chronic pain and failure of fixation can
occur particularly in the older patient.

The management of 3 or 4 part comminuted proximal humerus fractures is difficult and
controversial as both conservative and operative management can lead to disappointing results
with pain and/or loss of motion. The humeral head can undergo AVN leading to chronic pain.
Bone fragments may be thin and of poor quality and screws or wires may cut out leading to
failure of fixation. Shoulder replacement (usually a hemiarthroplasty for trauma) has been used
with the difficulty of reattaching the tuberosities and subsequent rotator cuff dysfunction. Range
of motion is often limited.

109

Head splitting fractures usually require shoulder replacement unless the patient is younger with
very good bone quality.

Shoulder(glenohumeral)dislocation

Anterior shoulder dislocation is much more common than posterior dislocation (only 25% of all
shoulder dislocations).

Traumatic anterior shoulder dislocation occurs due to an excessive external rotation force or a
fall onto the back of the shoulder. Dislocations can also occur due to a seizure (watch for bilateral
dislocations). Anterior dislocation often results in detachment of the anterior glenoid labrum and
capsule known as a Bankart lesion whilst the posterior humeral head can impact on the anterior
glenoid producing an impaction fracture of the posterior head (HillSachs lesion). The axillary
nerve can be stretched as it passes through the quadrilateral space whilst other nerves of the
brachial plexus as well as the axillary artery can be stretched or compressed.

Loss of symmetry is seen with loss of roundness of the shoulder and the arm held in an adducted
position supported by the patients other arm. The principle sign of axillary nerve injury is loss of
sensation in the regimental badge area. It may be difficult to determine deltoid contraction in the
acute phase. Full distal neurovascular assessment should be carried out. In older patients, tears
of the rotator cuff are very common but again these can be difficult to assess in the acute setting.

Figure 53: Normal shoulder (a); wasting of deltoid (b), dislocated shoulder with a positive
Hamilton's ruler sign where the ruler touches both the acromion and the lateral epicondyle (c);
acromioclavicular dislocation with a step at the acromioclavicular joint (d). Source: Dandy D and
Edwards DJ (2009).


Xrays confirm the injury. Fractures of the surgical neck and greater tuberosity can occur with
shoulder dislocation.

Closed reduction under sedation or anaesthetic is the mainstay of treatment with neurovascular
assessment before and after reduction. Radiographs are repeated to confirm reduction. The
patient is placed in a sling for 23 weeks to allow the detached capsule to heal then rehabilitation
with physiotherapy is commenced. Delayed presentation dislocations (eg alcoholics) may be
difficult to reduce by closed means and may require open reduction.

110

If there is an associated fracture of the greater tuberosity, this usually reduces to an acceptable
position with reduction of the shoulder however ORIF is usually required if it remains displaced.
Fracturedislocations involving the surgical neck usually require surgery.

The risk of recurrent dislocation is predicted by the age of the patient at the time of initial
dislocation. Patients less than 20 have an 80% chance of redislocation and many surgeons
advocate stabilization surgery after first time dislocation in this age group. Patients over 30 have
only a 20% risk of further dislocation and the redislocation rate reduced further with increasing
age. Recurrent dislocations can be stabilized by a Bankart repair with reattachment of the torn
labrum and capsule by arthroscopic or open means.

Some shoulder dislocations occur in patients with marked ligamentous laxity which may be
idiopathic generalized ligamentous laxity / hypermobility or due to a connective tissue disorder
(EhlersDanlos syndrome, Marfans syndrome). These patients tend to have atraumatic
multidirectional dislocations which can be painful (some can voluntarily dislocate as a party
piece). The results of surgery are less predictable due to the underlying biological component.
An open tightening of the shoulder capsule (known as a capsular shift) can improve stability but
the tightened capsule may stretch out again. Physiotherapy to strengthen the rotator cuff
muscles (which are secondary restraints to dislocation) is the mainstay of treatment.

Posterior shoulder dislocations are caused by a posterior force on the adducted and internally
rotated arm. The humeral head may be palpated posteriorly. They are often missed as the
radiographic findings are much less obvious than anterior dislocation. The main Xray finding is
the light bulb sign where the excessively internally rotated humeral head looks like a light bulb
on an AP view. Special lateral xray views assist in the diagnosis. Closed reduction and a period of
immobilization followed by physiotherapy are again the mainstay of treatment.

ACJointdislocation
Injuries of the acromioclavicular joint usually occur after a fall onto the point of the shoulder. The
joint can be sprained, subluxed (partially dislocated) or dislocated. With subluxations the
acromioclavicular ligaments are ruptured. If dislocated the coracoclavicular ligaments (conoid
and trapezoid ligaments) are also disrupted. Most injuries are treated with conservative
management wearing a sling for a few weeks followed by physiotherapy. Surgery (reconstruction
of the coracoclavicular ligaments) is reserved for those with chronic pain (although some
surgeons advocate early reconstruction for younger athletes with dislocation controversial).

Humeralshaftfracture
Humeral shaft fractures can be caused by direct trauma (RTA) resulting in transverse or
comminuted fractures, or by fall with or without twisting injury resulting in oblique or spiral
fractures. Union rates are high (90%) and due to the mobility of the ball and socket shoulder
joint proximally and the elbow joint distally, up to 30 of angulation can be accepted.
The radial nerve in the spiral groove is susceptible to injury which present with a wrist drop and
loss of sensation in the first dorsal web space.
Most cases are treated non-operatively with a functional humeral brace which compresses the
fragments into acceptable alignment and provides some stability.
Internal fixation with an intramedullary nail or plate and screws may afford a quicker recovery and
intramedullary nailing may be used in polytrauma. Non unions require plating and bone grafting.
Elbow
Supracondylarfractures
These fractures usually occur in children See childrens fracture section.

111

Intraarticulardistalhumerusfractures
As with most intraarticular fractures, these require ORIF with anatomic reduction and rigid
fixation to minimize loss of function. Special plates are available to follow the complex contours
of the distal humerus. Elbow replacement can be considered in highly comminuted fractures in
the elderly.
Olecranonfracture
Olecranon fractures are common and usually occur with a fall onto the point of the elbow with
contraction of the triceps muscle. Most fractures undergo ORIF to restore triceps function and
restore the articular surface. A simple transverse avulsion fracture can be fixed with tension
band wiring which compresses the tension side of the fractures. Comminuted fractures dont
have a fulcrum for the tension band and require ORIF with a plate and screws.
Radialhead&neckfractures
Radial head and neck fractures usually occur due to a fall onto the outstretched arm. Some
undisplaced fractures may not show up on xray other than a fat pad sign on the lateral xray (a
triangle like a sail anterior to the distal humerus) with lateral elbow pain on supination /
pronation.

Undisplaced or minimally displaced fractures are treated conservatively with a sling for comfort
followed by early elbow exercises to minimize stiffness. Patients often lose 1015 of terminal
extension. Displaced intraarticular radial head fractures may require surgery if the displaced
fragment causes a mechanical block to full extension. Aspitation of the haemarthrosis and
injection of local anaesthetic may help to exclude those with restricted ROM due to pain. ORIF is
performed if the fragment is large enough or excision if not amenable to fixation.
Elbowdislocation&fracturedislocation
Most elbow dislocations occur in the posterior direction after a fall onto the outstretched hand.
They may be associated with neurovascular injury. Uncomplicated dislocations require closed
reduction under sedation assessing neurovascular status pre and postreduction. A short period
in sling (13 weeks) followed by elbow exercises is typically required.

Associated fractures of the radial head, humeral epicondyles or coronoid process of the ulna may
occur. Surgery may be required if entrapped bony fragments prevent reduction or block motion.
Radial neck or head fractures may require ORIF or excision and replacement with a prosthetic
radial head to maintain stability. Epicondyle fractures are fixed with a screw. Large coronoid
fractures may need ORIF with small screws to prevent recurrent dislocation. Some cases with
recurrent instability may be helped with lateral elbow ligament reconstruction.
Forearmfractures

Principlesofforearmfractures
The forearm consists of the radius and ulna bones which are connected proximally and distally
by strong ligaments around the proximal and distal radioulnar joints where supination and
pronation occur. Because of these strong ligaments, the forearm acts as a ring where if one bone
is fractures, there is usually a fracture or dislocation involving the other bone. If an isolated
displaced fracture of one of the forearm bones is identified, one should have a very high index of
suspicion of a fracture or dislocation involving the other bone.
FractureoftheUlnarshaft(Nightstickfracture)
Isolated fractures of the ulna can occur after a direct blow. The injury is known as a nightstick
fracture as historically many cases occurred after being hit by a truncheon (Nightstick). One must
be sure that there is no associated Monteggia injury (see below). Many cases are dealt with by
conservative management however ORIF may afford earlier return to function and may reduce
the risk of nonunion.
Fracturebothbonesofforearm
A diaphyseal fracture of both bones of the forearm in adults usually requires ORIF with plates
and screws as the injury is highly unstable and anatomic reduction is required to maximize

112

function and prevent deformity. In children minimally angulated fractures can be treated with
plaster only as a small degree of angulation will remodel as the child grows. Substantially
angulated fractures or displaced fractures with an intact periosteum (identified after reduction)
are only unstable in one direction and can be treated with MUA (if necessary) and plaster. If the
fracture is very unstable after reduction, flexible intramedullary nails can be used.
MonteggiaFracturedislocation
This injury is where a fracture of the ulna occurs with dislocation of the radial head at the elbow.
Forearm xrays may not easily demonstrate the incongruence of the radiocapitallar joint and
therefore with isolated ulna fractures it is advisable to perform elbow xrays. The injury requires
ORIF of the ulna fracture (even in children) which should result in reduction of the radio
capitellar joint. Manipulation alone risks redislocation due to the unstable nature of the injury.
Galeazzifracturedislocation
The other forearm fracture dislocation is a fracture of the radius with dislocation of the ulna at
the distal radioulnar joint. Again the forearm xrays may not clearly demonstrate the dislocation
therefore with any isolated radial shaft fracture, a lateral xray of the wrist is mandatory. ORIF of
the radius is required which should allow the DRUJ to reduce.
Distalradiusfractures
Collesfracture
A Colles fracture is an extraarticular fracture of the distal radius within an inch of the articular
surface and with dorsal displacement or angulation. It occurs due to a FOOSH with the wrist
extended. The Dubliner Abraham Colles described the injury in 1814 from clinical findings before
xrays were invented (1895). Often there is an associated fracture of the ulnar styloid.

Treatment depends on the degree of displacement or angulation, the presence of dorsal
comminution and the functional demand of the patient. Fractures which heal with less angulation
and shortening tend to have a better outcome in terms of pain, grip strength, ROM, and function
(however this is not always the case and some seemingly malunited fractures can be pain free
with surprisingly good function despite the deformity).

Minimally displaced or angulated fractures may be treated with splintage alone but any
angulation past neutral (the distal radius articular surface is normally 10 volarly angulated) is
usually corrected by manipulation. The fracture may be held with a plaster cast alone or if the fracture
has dorsal comminution or is felt to be particularly unstable after reduction, percutaneous wires may be
used to pin the distal fragment in place or ORIF with plate & screws may be preferred.
Median nerve compression from stretch of the nerve or a bleed into the carpal tunnel can
accompany a Colles fractures. Reduction may relive the pressure on the nerve and the fracture is
usually stabilized with fixation. The carpal tunnel may need surgically decompressed.

A specific late local complication of Colles fractures is rupture of the Extensor Pollicis Longus
tendon (which usually requires a tendon transfer).
Smithsfracture
This is a volarly displaced or angulated extraarticular fracture of the distal radius which usually
occurs after falling onto the back of a flexed wrist. (Robert) Smith was also a Dubliner and again
the injury was described before the advent of Xrays (fracture described in 1847).

All Smiths fractures should undergo ORIF using a plate and screws as they are highly unstable
injuries. Also grip strength and wrist extension are greatly reduced if there is a malunion with
excessive volar angulation.
Bartonsfracture
Bartons fractures are intraarticular fractures of the distal radius involving the dorsal or volar
rim where the carpal bones of the wrist joint sublux with the displaced rim fragment. These
injuries require ORIF.

113

Comminutedintraarticulardistalradiusfracture
Some distal radius fractures are so comminuted (due to high energy or poor bone quality) that
stable fixation of the joint fragments is not possible. To restore the shortening and hold the wrist
in reasonable alignment and therefore limit functional deficit, an external fixator can be sited
across the wrist joint. Supplementary wires can be used to pin larger fragments in place.
Scaphoid&carpus
Scaphoidfracture
Scaphoid fractures usually occur after a FOOSH. Clinical signs include tenderness in the anatomic
snuff box (between APB/EPB & EPL tendons) and pain on compressing (telescoping) the thumb
metacarpal.

Due to the complex kidney bean shape of the scaphoid, fractures can be difficult to visualize on x
ray and 4 views are taken if scaphoid fracture is suspected (AP, lateral and 2 oblique views).
Around 5% of scaphoid fractures are not visible on initial xrays but show up on radiographs 2
weeks later after resorption of the fracture ends as the first stage of fracture healing.

If a scaphoid fracture is suspected clinically but the xray fails to demonstrate a fracture, the
wrist is splinted and further clinical assessment +/ further xray is arranged around two weeks
after the injury. The injury is referred to as a clinical scaphoid fracture.

Undisplaced fractures are usually treated with plaster cast for 612 weeks.

Scaphoid fractures can run into problems of nonunion (due to synovial fluid inhibiting fracture
healing) and avascular necrosis of the proximal pole (as its blood supply comes distally from a
branch of the radial artery). Displaced fractures should be fixed with a special compression
screw sunk into the bone to avoid nonunion. CT scan may be useful to determine if union has
occurred. Nonunions are treated with screw fixation and bone grafting. AVN once established is
difficult to treat and if patients are symptomatic partial or total wrist fusion may be required.
Perilunatedislocation&Lunatedislocation
Perilunate dislocation is an uncommon but severe high energy wrist injury resulting from
hyperdorsiflexion. Perilunate dislocation is a classic missed diagnosis with up to 25% of cases
being missed on initial presentation. Inexperienced or unwary clinicians may concentrate on the
lack of a distal radius fracture on radiographs whilst the dislocation of the capitate and other
surrounding carpal bones from their association with the lunate is not as obvious as one would
expect. Xrays demonstrate loss of alignment of the capitate and lunate with the concave lunate
fossa being empty. There may be an associated fracture through the scaphoid (a transscaphoid
perilunate dislocation) and other carpal bones. Median nerve injury / acute carpal tunnel
syndrome may be present.

Emergency treatment is required with closed reduction and percutaneous pinning or open
reduction if closed reduction is not possible. Ligament repairs can also be performed with open
reduction. Carpal tunnel decompression may also be required.

Lunate dislocation is a similar high energy injury where the lunate dislocates (usually volarly)
whilst the remainder of the carpal bones remain enlocated. The classic radiographic sign is the
spilt cup sign of the lunate which is usually tilted volarly and empty like a split tea cup. Again
median nerve compression is common. Treatment is similar with emergent closed +/ open
reduction and pinning.
Scapholunatedissociation
Scapholunate dissociation occurs when the scapholunate ligaments fail resulting in an
increased gap between the scaphoid and lunate on the AP xray and a hyperflexed scaphoid with a
dorsally tilted lunate.

If left untreated, abnormal forces are placed upon the wrist and carpus and osteoarthritis ensues.
Treatment is surgical with closed reduction and kwiring with or without scapholunate ligament

114

repair. Chronic cases without OA may be treated with soft tissue tethering to the distal pole of the
scaphoid to prevent hyperflexion (dorsal capsulodesis). Once OA is present partial or total wrist
fusion may be required to improve symptoms.
HandTrauma

Penetratinghandinjuries
Penetrating injuries to the hand from sharp objects are common. Volar injuries risk damage to
the flexor tendons, digital nerves and digital arteries. Dorsal injuries risk damage to the extensor
tendons. Thorough examination is required with assessment of neurovascular and tendon
function. One should have a very low threshold for surgical exploration as a tendon may appear
to function satisfactorily with only a small proportion in continuity risking subsequent rupture.

Complete or significant partial tendon injuries require surgical repair. Digital nerve injuries
proximal to the DIPJ warrant repair with sensation to the thumb, index and little fingers
particularly important. A history of an arterial injury (pulsatile bleeding) to a digit has a high
chanch of concurrent injury to the adjacent digital nerve. Whilst the circulation to the tip of a
digit may be fine with loss of one digital artery, injuries to both digital arteries requires
microsurgical repair to restore circulation.
Extensortendoninjuries
Extensor tendon divisions of 50% or more usually require surgical repair with splintage in
extension for 6 weeks as flexion may cause failure of the repair

Malletfinger
Mallet finger is an avulsion of the extensor tendon from its insertion into the terminal phalanx
and is caused by forced flexion of the extended DIPJ, often from a ball at sport. The patient
presents with pain, a drooped DIPJ of the affected finger and inability to extend at the DIPJ. The
injury may be a purely tendinous avulsion or may have a bony fragment.

Treatment is with a mallet splint holding the DIPJ extended which should be worn continuously
for a minimum of 4 weeks.
Flexortendoninjuries

Flexor tendon injuries in the fingers pose a particular problem as the tendons need to run
smoothly within the tendon sheath and under the pulleys (thickenings of the tendon sheath
which serve to hold the tendon into the finger). The digital nerves and arteries run adjacent to
the tendons in their sheaths and are also at risk of injury. Injuries can occur to the superficial
tendon (FDS), the deep tendon alone (FDP) if the injury is distal to the insertion of FDS, or both.
In the thumb the FPB tendon can be injure in its tendon sheath.

All palmar penetrating injuries of the fingers should be explored. Partial divisions with a flap of
tendon should be smoothed whilst significant partial lacerations or complete tendon divisions
require repair. The repair should be a smooth as possible with special suture techniques to
provide strength to the repair. The tendon sheath requires careful repair with preservation of the
pulleys to avoid bowstringing of the tendon. The fingers are splinted in a flexed position, often
with elastic traction to allow early active gentle extension and passive flexion to prevent stiffness
and adhesions within the tendon sheath.

Flexor tendon injuries in the palm may also require repair and may also have concomitant injury
to the interdigital nerves or arterial system. Penetrating injuries in the volar forearm risk injury
to the wrist flexors (FCU & FCR) as well as the long flexors to the fingers and thumb requiring
repair. Injuries can also occur to the median and ulnar nerves as well as the radial and ulnar
arteries (loss of both requires urgent surgical revascularization).

115

Metacarpalfractures
Fractures of the 3rd, 4th and 5th metacarpals are usually treated conservatively. The 3rd and 4th
metacarpals have strong intermetacarpal ligaments proximally and distally giving stability to
these fractures and usually minimal displacement.

Fractures of the 5th metacarpal often occur with a punching injury, particularly 5th Metacarpal
neck fractures (known as Boxers fractures). Up to 45 of angulation can be tolerated without
affecting hand function. Treatment is by neighbor strapping of the affected digit to the adjacent
finger and early motion to maintain function. Rotational alignment should be checked to avoid
problems with grip and any overlapping of the fingers when making a fist should be corrected by
manipulation with neighbor strapping or kwire stabilization.

With punching injuries a fight bite may occur with a laceration from a tooth which could
potentially penetrate the MCP joint and or disrupt the extensor tendon. Intraoral organisms may
cause an aggressive infection leading to septic arthritis and any suspected fight bite should be
explored and thoroughly washed out in theatre.

Phalangealfractures
Many phalangeal fractures can be treated with neighbour strapping or splintage. Significantly
displaced or angulated fractures may require manipulation under anaesthetic or digital nerve
block (ring block) and unstable fractures may require Kwiring or fixation with small screws.
Intraarticular fractures may be fixed with kwires or small screws.
Hip
Femoralneckfractures

Hip fractures are generally osteoporosis related in the elderly population. With the ageing
population numbers of hip fractures continue to rise. In 2007 there were more than 6300 hip
fractures in Scotland.

The majority of patients are over 80 years old with more than 75% being female. The lifetime
risk of sustaining a hip fracture for over 50 year olds is between 5 and 10% for males and 15
20% for females.

Many patients have significant comorbidites (cerebrovascular insufficiency, cardiac
arrhythmias, postural hypotension etc.) which contribute to their risk of falling. Comorbidities
(cardiorespiratory disease, renal failure et.c) and reduced physiological reserves also contribute
to risk of medical complications after surgery and the risk of such complications is fairly high
with risk of chest infections, respiratory failure, MI and acute renal failure. Mortality from hip
fracture is around 10% at one month, 20% at four months and 30% at one year.

Despite the risk of medical complications with surgery, nearly all patients with a hip fracture
undergo surgery as the risks of nonoperative management are just as high. With nonoperative
management, prolonged bed rest for several weeks would be required during which time the
patient would be very sore for toileting and bathing whilst they would be at very high risk of
problems with recumbency (pressure sores, chest infections) and the fracture may not heal.
Prolonged bed rest would also result in muscular atrophy making subsequent rehabilitation
difficult. Therefore to maximize the chance of restoration of function and to promote early
mobilization almost all hip fractures undergo surgery within the first 24 hours unless time is
required for medical optimization. The exceptions would be very high risk patients who are
expected to die in the short term. Despite early surgery approximately 20% of hip fracture
patients fail to regain independence and require long term care whilst 30% fail to return to their
preinjury function. Many patients require to use a stick or walking frame to aid mobility whilst
some fail to recover such that they need a wheelchair and may require assistance or a hoist to
transfer from bed to chair.

116

Hip fractures are broadly classified as being intracapsular or extracapsular. The arterial supply
of the femoral head comes from a ring anastomosis of the circumflex femoral arteries at the
insertion of the hip capsule at the base of the femoral neck. The medial and lateral circumflex
femoral arteries are branches of the profunda femoral artery. Arteries from the ring anastomosis
travel up the femoral neck and into the femoral head.

Intracapsular hip fractures can therefore interfere with the arterial supply of the femoral head
and risk avascular necrosis and nonunion. These fractures are more reliably treated with a
replacement femoral head which can either be a hemiarthroplasty (replacing the femoral head
alone) or total hip replacement (replacing the acetabulum as well as the femoral head). Total hip
replacement has a higher risk of dislocation (particularly in the cognitively impaired) but can
give better function and is reserved for the higher functioning hip fracture patient with hemi
arthroplasty generally preferred for the those with restricted mobility and the cognitively
impaired patient.

Extracapsular hip fractures should not cause avascular necrosis and have a high union rate.
These farctures can therefore be fixed with a Dynamic Hip Screw (DHS) keeping the patients
own natural hip joint. The DHS is dynamic in that the screw in the femoral head and neck is
allowed to slide in the barrel of the plate applied to the femoral shaft which results in
compression at the fracture site which promotes fracture healing. The fracture usually heals in a
shortened position.
Subtrochantericfractures

Subtrochanteric fractures also usually occur in the elderly patient with osteoporosis and a fall
onto the side.

The subtrochanteric bone has a relatively poor blood supply and is an area of bone under
considerable bending stress. Fractures take a while to heal and nonunion occurs fairly
frequently. Strong indirect fixation without further disruption to the blood supply in the form of
an intramedullary nail is recommended.

Preoperative pain relief and stabilization of the fracture may be helped with application of a
Thomas splint (see below).
Femoralshaftfracture

Femoral shaft fractures usually occur as high energy injuries and as such there a substantial risk
of concomitant fracture elsewhere. Stress fractures of the femoral shaft can also occur in
osteoporotic bone, metatstatic disease, patients with Pagets disease and paradoxically with long
term bisphosphonate use for osteoporosis.

With displaced femoral shaft fractures substantial blood loss of up to 1.5l can occur. Fat from the
medullary canal can enter the damaged venous system resulting in fat embolism with confusion,
hypoxia and risk of ARDS.

Initial management after initial resuscitation includes optimizing analgesia with a femoral nerve
block and application of a Thomas splint which stabilizes the fracture minimizing further blood
loss and fat embolism.

Definitive management is usually closed reduction and stabilization with an intramedullary nail
however minimally invasive plate fixation with minimal disruption to the fracture site blood
supply can also be used.
Knee
Distalfemurfracture

117

Distal femur fractures usually occur in osteoporotic bone with a fall onto the flexed knee.
Fractures can be extraarticular (supracondylar) or intraarticular (intercondylar). The distal
fracture usually adopts a flexed position (due to the pull of the gastrocnemii muscles) and unless
the patient is very frail and not fit for surgery, these fractures are usually fixed with a plate and
screws as the fracture position is difficult to maintain in a cast.
Kneedislocation

Knee dislocations are uncommon but can occur in high energy injuries or with severe
hyperextension and/or rotational forces with a sporting injury. A knee dislocation is a surgical
emergency with a high incidence of vascular injury (intimal tears, vascular occlusion, complete
transection), nerve injury and compartment syndrome.

Frank dislocations should be reduced urgently with thorough neurovascular assessment and
vascular surgery referral if any doubt with further investigation (Doppler, duplex scan or
angiogram) and revascularization (endovascular procedures or bypass) as required. If the knee is
very unstable an external fixator may be applied. Multiligament reconstruction is typically
required once the soft tissue envelope has settled. Knee injuries with evidence of gross instability
(particularly PCL and LCL injuries from hyperxtension & varus) may have been true dislocations
with spontaneous reduction and careful attention should be paid to the neurovascular status.

Patellardislocation

Patellar dislocations are relatively common. Virtually all are lateral dislocations due to either a
direct blow (e.g. clash of knees at sport)or a contraction of the quadriceps with a rotational force
with the patella not engaged in the trochlea (less than about 30 flexed). The patella may remain
dislocated requiring manipulation for reduction or may spontaneously reduce. Subluxations can
also occur without frank dislocation.

Patellar dislocations and subluxations are more common in adolescents, particularly females and
are predisposed to by generalised ligamentous laxity valgus or rotational malalignment
(including femoral neck anteversion) and a shallow trochlear groove. Patients have tenderness
over the medial retinaculum (where the medial patellofemoral ligament is torn) and may have a
haemarthrosis from impaction of the medial patellar facet on the outer aspect of the lateral
femoral condyle. Osteochondral fractures can occur with sheared off / detached fragments
occasionally requiring retrieval or fixation depending on their size and amount of bone on the
detached fragment.

Around 10% of all first time patellar dislocation patients will experience a further dislocation and
50% of those will have multiple recurrent dislocations. Temporary splintage followed by
physiotherapy (to strengthen the vastus medialis) can help prevent further dislocations and
many adolescent patients stabilize as they get older. Occasionally surgical stabilization with
either a bony procedure for malalignment or a soft tissue (MPFL) reconstruction is required.
Proximaltibia/tibialplateaufracture

Tibial plateau fractures can be either high energy injuries in the younger patient or low energy in
osteoporotic bone. They are intraarticular fractures with either a split in the bone, a depression
of the articular surface or a combination of both. High energy injuries may have associated
neurovascular injury or compartment syndrome. As with most intraarticular fractures, surgery
is usually required with the aim of reduction of the articular surface and rigid fixation with early
motion to combat the risk of stiffness and post traumatic OA. CT scans are useful to plan surgical
fixation.

A valgus stress injury to the knee may cause a lateral plateau fracture with failure of the MCL and
possibly ACL with increasing force. A direct blow from a car bumper may also cause proximal
fibular fracture and injury to the common peroneal nerve with footdrop. A varus injury may

118

result in a medial plateau fracture (less common) with potential for LCL rupture and stretch
injury to the common peroneal nerve.

Plates and screws are usually used for fixation. Once a depressed fracture has been elevated, a
void in the bone is left requiring bone grafting (usually morsellised packed cancellous autograft
from the iliac crest) to provide support.

With high energy fractures there is often substantial soft tissue swelling and temporary external
fixator spanning the joint may be required for initial stability and to allow the swelling to resolve
before embarking on definitive open reduction and internal fixation. Some surgeons use external
fixation for the definitive management of these injuries using a ring fixator and fine wires under
tension to hold fracture fragments.

Despite efforts to restore the articular surface, results of surgery are often disappointing and
patients often require subsequent Total Knee Replacement.
Tibialshaftfracture

Tibial shaft fractures usually occur with indirect force and either bending (transverse fracture)
or rotational energy (spiral fracture), compressive force from deceleration (oblique fracture), a
combination of these forces or from high energy injuries (comminuted fracture).

Open fractures are not uncommon due to the tibial shaft being subcutaneous and tibial fractures
are the commonest cause of compartment syndrome after trauma (particularly the anterior
compartment of the leg).

Up to 50% displacement and 5 of angulation in any plane can be accepted with conservative
management in an above knee cast. Any internal rotation of the distal fragment is poorly
tolerated. The position may be difficult to control in a cast with frequent cast changes and check
xrays required. If the fibula is not fractured, the tibia often drifts into varus whilst if the fibula is
also fractured valgus alignment is more common. Internal fixation controls the position of the
fracture and removes the need for a cast with the benefits of early joint motion and a potentially
quicker rehabilitation.

There are several different ways to treat tibial shaft fractures with no single best method.

Conservative management avoids the risk of surgery but it may be difficult to maintain the
fracture position. The tibia is one of the slowest healing bones in the body with average time to
union of around 16 weeks and can take up to a year to heal.

Comminuted fractures are highly unstable and generally require surgical stabilization. Open
fractures require surgical stabilization as previously discussed and plastic surgical assistance
may be required to ensure adequate skin coverage. Compartment syndrome requires urgent
fasciotomies and surgical stabilization of the fracture.

ORIF with plates and screws gives rigid stability but dissection down to the fracture site further
reduces the peristeal blood supply to the fracture site and may risk nonunion.

Intramedullary nailing is the commonest method of surgical stabilization and promotes
secondary bone healing with less disruption of the periosteal blood supply to the fracture site.
The nail is inserted behind the patellar tendon and around 25% of patients suffer significant
anterior knee pain.

External fixation is favoured by some but problems can occur with pin site infection and/or
loosening.

Non unions may require bone grafting or special circular frames which can be adjusted to alter
angulation, rotation or length, can give compression at the fracture site to promote healing and
can form new bone from distraction osteogenesis.

119

Distaltibia&Pilonfractures

Extraarticular fractures of the distal tibia in an acceptable position can be treated with either
conservative management if the position is acceptable or surgical stabilization with early motion.
If the fracture is not too distal an intramedullary nail can be used however if the fracture is too
distal to accommodate the distal locking screw(s) of a nail, plating is preferred.

Intraarticular fractures of the distal tibia generally require ORIF to ensure a congruent articular
surface.

Pilon fractures are high energy fractures of the distal tibial plafond cause by a fall from height or
rapid deceleration. A pilon is a pestle in French (as is mortar and pestle) and with a pilon
fracture the talus acts like a pestle and is driven into the distal tibial articular surface (the
mortar) causing usually substantial disruption, comminution or impaction of the articular
surface. These are high energy injuries with substantial soft tissue swelling, a high incidence of
other injuries. Pilon fractures are surgical emergencies treated with very early internal fixation if
the soft tissue envelope is satisfactory or in most cases with temporary external fixation with
delayed internal fixation once the swelling settles. CT scans are often required to plan fixation
and the surgical approach to be used. Impacted articular surface fragments need to be retrieve
and any voids filled with bone graft.

Ankle arthrodesis may be required for posttraumatic OA.
Ankle

Ankle injuries are very common with most being due to an inversion injury and/or rotational
force on a planted foot.

Sprains of the lateral ankle ligaments (anterior & posterior talofibular ligaments and
calcaneofibular ligament) are commonplace and are characterized by pain, bruising and mild to
moderate tenderness over the involved ligaments. With higher force / energy or in osteoporotic
bone, fractures occur.

In A&E the Ottawa criteria are used to identify a suspected ankle fracture and give guidance as to
which ankle injuries require an Xray. Any severe localized tenderness (known as bony tenderness
of the distal tibia or fibula or inability to weight bear for four steps merits an xray.

With ankle fractures a distinction needs to be made between stable and unstable fractures.
Isolated distal fibular fractures with no medial fracture or rupture of the deltoid ligament are
stable and are common. Treatment is with a walking cast or splint for around 6 weeks. Distal
fibular fractures with rupture of the deltoid ligament are unstable and usually undergo ORIF
(with plates and screws). Rupture of the deltoid ligament is suspected by bruising and
tenderness medially. If there is any talar shift ocurring on a mortise AP view xray (with the foot
slightly internally rotated) where there is asymmetric increased space around the talus within
the ankle mortise (a mortise is a rectangular recess like in a mortise lock) or talar tilt with the
talus and tibial plafond being non parallel, then by definition the deltoid ligament must be
ruptured if there is no medial malleolar fracture. Ankle joint contact pressures greatly increase
with even 1mm of talar shift with subsequent risk of post traumatic OA. Therefore anatomic
reduction and rigid internal fixation is required to minimize this risk with any talar shift. Gross
talar shift results in a fracturedislocation (rather than a fracturesubluxation).

Bimalleolar fractures are unstable and usually undergo ORIF

Ankle fractures can be associated with substantial soft tissue swelling and fracture blisters. ORIF
may be delayed by 12 weeks to allow the soft tissues to settle and reduced the risk of wound
healing problems and infection.

120

Foot
Calcanealfractures

Calcaneal fractures occur due to fall from height onto the heel (eg fall from ladder). Other injuries
associated with a fall from height should be excluded (especially spinal injuries).

Fractures can be extraarticular or can involve the subtalar joint. There may be substantial soft
tissue swelling and compartment syndrome of the foot can occur. Prognosis is dependant on the
extent of involvement of the subtalar joint and the degree of comminution. The heel tends to drift
into a valgus position with a widened heel causing impingement of the lateral ankle tendons.

Treatment is controversial. Whilst many surgeons advocate ORIF to restore the articular surface
in the younger patient, there is a risk of wound healing problems and if wound breakdown occurs
it can be difficult to achieve skin coverage without problems from footwear. Heavy smoking,
vascular disease, diabetes, poor surgical technique and increasing age increase the risk of wound
healing problems and infection. There is also no evidence to date that ORIF improves pain or
function long term.

For those who develop chronic pain due to subtalar joint damage or OA, subtalar arthrodesis is
an option.
Talusfractures

Fractures of the talar neck usually occur with forced dorsiflexion from rapid deceleration (RTA,
aircraft crash). Fractures can be undisplaced or displaced with subluxation of the subtalar joint.
Higher energy injuries may also result in dislocation of the body of the talus from the ankle joint
or the head of the talus from the talonavicular joint.

The body if the talus gains its blood supply from distally with anastomoses around and vessels
traversing the talar neck. With displacement and subluxation / dislocation there is a high risk of
AVN affecting the talar body.

Treatment of displaced fractures is by closed or open reduction and screw fixation. AVN of the
talus is not always symptomatic but secondary symptomatic OA may require ankle fusion.

Midfoot(Lisfranc)fracturedislocation

This is an uncommon but often overlooked injury where a fracture of the base of the 2nd
metatarsal is associated with dislocation of the base of the 2nd metatarsal with or without
dislocation of the other metatarsals at the tarsometatarsal joints. The ligament from the medial
cuneiform to the base of the 2nd metatarsal no longer holds the bone in joint. The fracture may
only be a small flake fracture which can be easily missed and the dislocation can be difficult to
appreciate on standard Xrays. A CT scan is required if there is any doubt.

Untreated, these injuries have a fairly high risk of pain and disability and therefore to reduce this
risk closed or open reduction with fixation using screws is recommended.

Metatarsalfractures

Fractures of the base of the 5th metatarsal are common and occur due to an inversion injury with
an avulsion fracture at the insertion of the peroneus brevis tendon. These heal predictably and
require a walking cast, supportive bandage or wearing of a stout boot for 46 weeks. Even with
those which fail to achieve bony union, many have a stable fibrous nonunion which is usually
asymptomatic.

121

With some injuries the bone fractures in the region of the proximal diaphysis where the injury is
known as a Jones fracture. These can be more problematic as this area has a relatively poor blood
supply and risk of nonunion is higher (around 25%) even in undisplaced farctures. Displaced
fractures or fractures in the very active may undergo fixation, usually with a single screw. Non
unions require bone grafting and fixation.

The first metatarsal is uncommonly fractured (due to its thickness and strength) but such is the
importance of the first ray to foot function that fractures of the first metatarsal are usually fixed.

The lesser metatarsals are commonly fractured, often with multiple fractures. With minimal
displacement these may be treated conservatively with a cast. Multiple displaced fractures may
be stabilized with Kwires to reduce the risk of chronic pain.

The 2nd metatarsal is a common site for a stress fracture. Fractures can occur spontaneously or
after a period of increased exercise / activity. The fracture may not be visible on plain xray until
a healing / callus response has started (can take several weeks). Bone scan may aid in the
diagnosis and treatment is with a cast until the pain subsides.

Toefractures

Toe fractures rarely require anything other than protection in a stout boot. Intraarticular
fractures of the base of the proximal phalanx of the hallux may benefit from reduction and
fixation if the fragment(s) are sizeable. Open fractures require debridement and may be
stabilized with a wire.

Dislocations are treated with closed reduction and either neighbor strapping or wiring.

Commonchildrensfractures

Fracturesofthedistalradius

Buckle fractures can occur which are stable and require only 34 weeks of splintage

Greenstick fractures may be angulated and may require manipulation and casting if there is
significant deformity, particularly in the older child

SalterHarris II fractures commonly occur around the distal radial physis in older children.
Angulation with deformity requires manipulation. Growth problems are highly unlikely (as with
most Salter Harris II fractures).

Complete fractures may displace as well as angulate with dorsal displacement and angulation
more common than volar. The dorsal periosteum usually remains intact which prevents
overcorrection of the deformity and aids stability. If the fracture is fairly stable, casting may
suffice. If a complete fracture is very unstable after reduction, wire stabilization or plate fixation
may be employed.

Childrensforearmfractures

Both Monteggia and Galeazzi fracturedislocations can occur in children and adults. These
injuries go against the usual principles of childrens fractures in that anatomic reduction and
rigid fixation with plates and screws is typically used as there is a high rate of redislocation of
the radial head or DRUJ with manipulation and casting.

With fractures of both bones of the forearm, angulated fractures usually have an intact
periosteum and the instability may only be in one plane which can be controlled with a cast after

122

manipulation. Displaced fractures tend to be unstable and flexible intramedullary nail are usually
used.

Supracondylarfractureoftheelbow

The supracondylar region of the distal humerus is a relatively weak point in the growing upper
limb and supracondylar elbow fractures are fairly common injuries. Extension type fractures are
more common and occur due to a heavy fall onto the outstretched hand. The less common flexion
type injury occurs with a fall onto the point of the flexed elbow.

Undisplaced fractures are stable and are treated with a splint.

Angulated, rotated or displaced fractures require closed reduction and pinning with wires to
prevent deformity. With severely displaced / offended fractures the brachialis muscle may be
tethered in the fracture site requiring open reduction if the fracture cannot be reduced by closed
means. With offended extension type fractures the distal fragment displaces posteriorly with
stretch and pressure on the brachial artery and median nerve (predominantly its anterior
interosseous branch the patient is unable to make the OK sign due to loss of FPL and FDP to
the index).

Displaced fractures should be reduced fairly soon to avoid swelling which can make reduction
more difficult. However, if the radial pulse is absent or reduced in volume, emergency surgery is
required. Closed reduction may be performed with wiring and the pulse may return if the artery
is no longer under stretch. However occasionally the brachial artery will be trapped in the
fracture site and if the hand remains pulseless after reduction, open surgical exploration is
required.

In the presence of a nerve injury, urgent theatre management is also required. The majority of
nerve injuries are neurapraxias which improve with time and occasionally an axonotmesis which
should also improve. Ongoing neuralgic pain (unpleasant shooting or burning pain radiating to
the sensory districution of the nerve) or no improvement may indicate entrapment of the nerve
which may require surgical release.

Femoralshaftfracture

Femoral shaft fractures can occur in children due to a fall onto a flexed knee or by indirect
bending or rotational forces.

With femoral shaft fractures in children, overgrowth tends to occur after fracture healing and
therefore some shortening can be accepted (more with younger children).

In children less than 2 years old more than half of femoral shaft fractures are due to NAI / child
abuse other signs of NAI should be looked for (see previous multiple injuries & bruises of
varying age, atypical injuries, inconsistent or inappropriate history etc.) and acted upon
appropriately. With patients less than 2 years old, treatment with Gallows traction and early hip
spica cast is appropriate.

With patients aged between 2 and 6, options include a Thomas splint or a hip spica cast

For children between 6 and 12 the femur is large enough to accommodate flexible intramedullary
nails which obviate the need for traction or cast.

For children aged 12 and above, an adult type intramedullary nail is typically used.

One should remember that the femur is a common site for benign and malignant bone tumors
and the fracture may be pathological with osteolysis and cortical thinning.

123

Tibialfractures

Undisplaced spiral fractures of the tibial shaft are common in toddlers (the injury is known as a
toddlers fracture) and these require a short time in cast.

Management in a cast is the mainstay for the majority of childrens tibial fractures. The risk of
compartment syndrome is much less than that for an adult. Up to 10 of angulation may be
accepted and greater degrees of angulation may be treated with manipulation and casting. Serial
xrays in the cast are required to ensure that the fracture does not drift into excessive angulation
in the AP or lateral planes. Shortening or malrotation should not be accepted.

Options for stabilizing very unstable or open fractures include flexible intramedullary nails,
plates and screws or external fixation. Adolescents with a closed proximal tibial physis can hav
an adult type intramedullary nail.

124

References:

3 Point Products. 2011. My Toes are Crooked Part 3: Hammertoes [Online]. Available:
http://www.3pointproducts.com/bloghealtharthritisfingerandtoe
conditions/bid/61800/MyToesareCrookedPart3Hammertoes [Accessed 16th July
2013].
3tailer. Resolve Halo MRSafe System [Online]. Available: http://www.3tailer.com/resolvehalo
mrsafesystem [Accessed 16th July 2013].
American College of Rheumatology. 2011. Osteoarthritis: Heberden's and Bouchard's Nodes,
Fingers
[Online].
Available:
http://images.rheumatology.org/viewphoto.php?albumId=77030&imageId=2897683
[Accessed 2013 16th July].
American Society for Surgery of the Hand. 2012. Dupuytren's Disease [Online]. Available:
http://www.assh.org/Public/HandConditions/Pages/DupuytrensDisease.aspx
[Accessed 13th July 2013].
Bass A 2012. Update on club foot. Paediatrics and Child Health, 22, 239 242.
Berger RA & Weiss APC 2003. Hand Surgery, Lippincott Williams & Wilkins, 9780781728744.
Dandy D & Edwards DJ 2009. Essential Orthopaedics and Trauma, 5th, Churchill Livingstone, 978
0443067181.
Dent J 2011. The Case of Squashed Nerve. University of Dundee.
Douglas G, Nicol F & Robertson C 2009. Macleod's Clinical Examination, 12th, Churchill
Livingstone, 9780443068485.
Eorthopod. 2009. A Patient's Guide to Rotational Deformities in Children [Online]. Available:
http://www.eorthopod.com/content/rotationaldeformitiesinchildren [Accessed 13th
July 2013].
Fauci A, Kasper D, Braunwald E, Hauser S, Longo D, Jameson J & Loascalzo J. Harrison's Principles
of Internal Medicine: Osteoarthritis [Online]. The McGrawHill Companies. Available:
http://dualibra.com/wp
content/uploads/2012/04/037800~1/Part%2014.%20Disorders%20of%20the%20Im
mune%20System,%20Connective%20Tissue,%20and%20Joints/Section%203.%20Diso
rders%20of%20the%20Joints%20and%20Adjacent%20Tissues/326.htm
[Accessed
13th July 2013].
French LM & Dietz FR 1999. Screening for Developmental Dysplasia of the Hip. American Family
Physician, 60, 177 184.
Gerber JR, Wilks T & ErdieLalena C 2010. Developmental Milestones: Motor Development.
Pediatrics in Review, 31, 267 277.
Harb A, Shawwa K, Airaiyes AH & Airaies CM 2013. Severe Rheumatoid Arthritis Hand Deformity.
BMJ Case Reports.
Haspi Medical Anatomy & Physiology. Long Bone Immobilization [Online]. Available:
http://www.haspi.org/curriculumlibrary/APCore
Labs/00%20Med%20A%20&%20P%20Core%20Labs%20618
13/08e%20Long%20Bone%20Immobilization.pdf [Accessed 17th July 2013].
King MH 1987. Primary Surgery: Volume 2: Trauma, OUP Oxford, 9780192615985.
Kumar P & Clark M 2012. Kumar and Clark's Clinical Medicine, 8th, Saunders Ltd, 978
0702044991.
LeidigBruckner G & Grauer A 1998. Blue Sclerae in Osteogenesis Imperfecta. The New England
Journal of Medicine, 339.
Luqmani R, Porter D & Joseph B 2013. Textbook of Orthopaedics, Trauma and Rheumatology, 2nd,
Mosby, 9780723436805.
Macdonald A 2011. Lecture 1 The Upper Limb. University of Dundee.
Marchessault JA, Mckay PL & Hammert WC 2011. Management of Upper Limb Amputations. The
Journal of Hand Surgery, 36, 1718 1726.
Miller MD 2012. Review of Orthopaedics, 6th, Saunders, 9781437720242.
Muchow RD, Flannery WD, Miedaner JA, Noonan KJ & Mccarthy JJ 2010. Compartment Syndrome
After Serial Casting in Spatic Diplegic Cerebral Palsy: A Case Report. Archives of Physical
Medicine and Rehabilitation, 91, 653 655.

125

Pediatric Orthopedics. 2010. Birth palsies (brachial plexus injuries) [Online]. Available:
http://pediatricorthopedics.org/orthopedicconditionsfrombirthtowalking/24
birthpalsiesbrachialplexusinjuries.html [Accessed 11th July 2013].
Reeder J & Orwoll E 2006. Adults with Osteogenesis Imperfecta. The New England Journal of
Medicine, 355.
Schmidt OI, Gahr RH, Gosse A & Heyde CE 2009. ATLS and damage control in spine trauma. World
Journal of Emergency Surgery, 4, 11.
Sinaiem. Pearls [Online]. Available: http://www.sinaiem.org/pearls/2013/05/31/1979/
[Accessed 2013 16th July].
Smith
E.
Innovations
in
Total
Hip
Replacement
[Online].
Available:
http://evertsmith.com/innovations/ [Accessed 11th July 2013].
Staker
B.
2013.
Osteoporosis
Awareness
Month
[Online].
Available:
http://stakerchiro.com/osteoporosisawarenessmonth/ [Accessed 11th July 2013].
Sugathan HK & Sherlock DA 2009. A Modified Jones Procedure for Managing Clawing of Lesser
Toes in Pes Cavus: Longterm Followup in 8 Patients. The Journal of Foot and Ankle
Surgery, 48, 636 641.
Sun M, Ma F, Zeng X, Liu Q, Zhao XL, Wu FX, Wu GP, Zhang ZF, Gu B, Zhao YF, Tian SH, Lin B,
Kong XY, Zhang XL, Yang W, Lo WHY & Zhang X 2008. Triphalangeal thumb
polysyndactyly syndrome and syndactyly type IV are caused by genomic duplications
involving the long range, limbspecific SHH enhancer. Journal of Medical Genetics, 45, 589
595.
Taniegra ED 2004. Hyperparathyroidism. American Family Physician, 69, 333 339.
Underwood JCE 2009. General and Systematic Pathology, 5th, Churchill Livingstone, 978
0443068881.
Velvet Deer Antler. Nerve Damage: Causes, Symptoms and Treatment [Online]. Available:
http://www.velvetdeerantler.org/explain/nervedamagecausessymptomsand
treatment/ [Accessed 16th July 2013].
Yale
Medical
Group.
Spina
Bifida
[Online].
Available:
http://www.yalemedicalgroup.org/stw/Page.asp?PageID=STW026778 [Accessed 11th
July 2013].

126