Most people with OA are managed in the primary care setting. However, if OA becomes severe with progressive limitation of functional and recreational activities, the opinion of an orthopaedic surgeon should be sought. Joint replacement is considered when conservative measures are unsuccessful and there is substantial impact on the person’s quality of life (refer to Chapter 14 for elective care and arthroplasty of the hip, knee and shoulder).

Spondyloarthropathies

Spondyloarthropathies (SpA) are a group of common inflammatory rheumatic disorders, characterised by axial and/or peripheral arthritis associated with enthesitis, dactylitis and potential extra-articular manifestations, such as uveitis and skin rash. These conditions share a common genetic predisposition – the HLA-B27 gene. Ankylosing spondylitis (AS) and psoriatic arthropathy are the two most common forms; Table 13.1 lists additional arthropathies.

Ankylosing spondylitis (AS)

AS is a systemic, chronic inflammatory disease that affects the axial skeleton, causing inflammatory back pain, which can lead to structural and functional impairment. The condition has an insidious onset, often over a period of several years, and typically occurs before the age of 30; usually between the late teens and twenties with a male to female ratio of 3:1 (Sieper et al., 2002). It affects men and women differently; women experience less severe disease with less involvement of the spine than men. However, women have more symptoms in the knees, wrists, ankles, hips and pelvis, whereas men most commonly experience involvement of the spine, pelvis, chest wall, hips, shoulders and feet (NASS, 2004). The cause is unknown. There are two central features: inflammation and new bone formation, especially in the spine. Although inflammation is assumed to trigger new bone formation, there is no close correlation between inflammation and osteoproliferation. The principle signs and symptoms include:

• Low back pain – of slow and gradual onset over several months and persistent in nature. Lower back pain in the lumbar spine and sacroiliac joints is often the initial complaint of approximately 90% of patients with the condition. Pain characteristically radiates to the buttocks or thighs, but never below the knee. Pain is worse in the morning or after a period of inactivity and may be relieved by mild physical exercise.
• Sacroiliitis (bi-lateral inflammation of the sacroiliac joints) – traumatic disease occurring at the point of attachment of skeletal muscles to bone, where recurring stress causes inflammation and often fibrosis and calcification.
• Stiffness – morning stiffness is a characteristic symptom, which may last for minutes to hours depending on disease severity and usually reduces during the day or is relieved by mild physical exercise.
• Enthesitis – inflammation at the point of attachment between skeletal muscles and bone.
• Peripheral arthritis – affecting about 10% of patients at presentation but eventually affects 40% of those with the condition. Peripheral arthritis is typically asymmetrical and predominantly affects the large joints of the appendicular skeletal system.
• Fatigue – some individuals may experience significant systemic symptoms including loss of weight during the early stages of disease, anaemia and depression.
• Acute anterior uveitis – inflammation of the eye occurs in 40% of patients on at least one occasion and 33% may experience recurring episodes which may lead to permanent damage and blindness if not treated promptly.
• Restricted spinal movement – occurs in all three planes (flexion, extension, rotation).
• Reduced costovertebral movement – results in reduced chest expansion and vital capacity.
• Invertible osteoporosis and associated spinal fractures.
• Aortic insufficiency.
• Atrial ventricle block.
• Pericarditis.
• Pulmonary fibrosis.

There are currently no specific diagnostic interventions; rather investigations may be used to exclude other potential diagnoses. Laboratory investigations include C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) which may be mildly elevated. Rheumatoid factor and antinuclear tests are negative with 95% of people with ankylosing spondylitis HLA-B27 positive. Although this is present in about 8% of the British population, most individuals will not have the condition although there is a strong familial tendency in people with ankylosing spondylitis. X-rays are diagnostic only in established cases with MRI imaging being a more helpful diagnostic tool.

Although AS is determined through clinical diagnosis, it is essential that alternative possible diagnoses are excluded, including mechanical back pain, infection, neoplasms and other inflammatory conditions. The British Society for Rheumatology (2004) advocates the use of the modified New York criteria (Geijer et al., 2009) as a guide to diagnosis. The four-point grading reports grade 0 as normal; grade I with some blurring of the joint margins as suspicious; grade II as having minimal sclerosis with some erosion; grade III as definite sclerosis on both sides of joint/severe erosions with widening of joint space with or without ankylosis; and grade IV as complete ankylosis. Therefore a definitive diagnosis of ankylosing spondylitis requires radiological criteria:

• when sacro-iliitis is greater than grade I bilaterally or grade III or IV unilaterally
• plus at least one clinical criterion from either:
  • low back pain and stiffness for more than three months that improves with exercise but is not relieved by rest
  • limited motion of the lumbar spine in both sagittal and frontal planes or
  • limited chest expansion compared to normal values correlated for age and sex.

A key element of the overall management for all patients is new evidence-based recommendations produced by the International Assessment in Ankylosing Spondylitis Working Group in collaboration with the European League Against Rheumatism (IAAS 2006). Physiotherapy may be beneficial but the best option is unclear. Many patients find hydrotherapy particularly beneficial. NSAIDs appear to improve spinal and peripheral pain and function along with intra-articular or peri-articular corticosteroid injections to the sacroiliitis in small groups. Local corticosteroid injections for peripheral arthritis and enthesitis in ankylosing spondylitis are widely used to good effect. Intravenous methylprednisolone is occasionally used in severe unresponsive cases, but this use may decline with the ability to use new medications like tumour necrosis factor inhibitors.

Drugs that inhibit tumour necrosis factor (TNF) have revolutionised the treatment of ankylosing spondylitis. Four different drugs are currently available:

• etanercept – a recombinant TNF receptor
• infliximab – a chimeric monoclonal antibody given by intravenous infusion
• adalimumab and golimumab – both humanised monoclonal antibody to TNF given subcutaneously.

These drugs have rapid and substantial clinical effects, in significantly reducing spinal inflammation. The British Society of Rheumatology (2004) and NICE (2008b) have produced guidelines for the use of TNF inhibitors.

A large proportion of patients with AS develop hip arthritis. Hip replacements should be considered in patients with refractory pain or disability and with radiographic evidence of structural damage, independent of age. Spinal surgery may be of value in selected patients and is performed for a variety of reasons, including fusion procedures for segmental instability and wedge lumbar osteotomy for fixed kyphotic deformity. Patients with severe ankylosing spondylitis present anaesthetic difficulties and the risk and benefits of surgery need to be carefully considered.

Psoriatic arthritis (PA)

PA is an inflammatory arthritis associated with the skin disorder psoriasis. The exact aetiology is unknown, although more than 40% of people with the cutaneous disease of psoriasis are estimated to also have joint involvement. Although some patients with psoriasis may have coincidental osteoarthritis or rheumatoid arthritis, it is important to remember that psoriatic arthritis is prevalent in individuals with psoriasis. Psoriasis is believed to affect 1–3% of the population and psoriatic arthritis is believed to affect 1% and affects more than 7–42% of patients with psoriasis. The risk of psoriatic arthritis increases with a family history of spondyloarthropathy or nail pitting and the onset usually occurs between 30 and 55 years of age, affecting men and women equally. Psoriatic arthritis is considered a separate entity from rheumatoid arthritis because of the sero-negativity of rheumatoid factor and its tendency for asymmetrical involvement.

The exact aetiology has yet to be discovered. As with almost all autoimmune diseases, genetic, immunological and environmental factors are believed to play a part in the expression of psoriatic arthritis. Psoriatic arthritis is an inflammatory disease that manifests in both articular and extra-articular features. The disease can present with an arthritis affecting several joints of the hands or feet that is frequently symmetrical. This mimics the pattern of rheumatoid arthritis. Unlike individuals affected by rheumatoid arthritis, those with psoriatic arthritis often experience inflammation of the distal interphalangeal joints. Individuals affected may also present with inflammation of the spine and sacroiliitis. The disease can also present with a dactylitis: sausage-like digit or digits. Individuals with psoriatic arthritis can have arthritis of less than four joints, commonly of one large joint and three digits, or an arthritis affecting one joint, usually a large joint. Uncommonly, psoriatic arthritis can be an extremely aggressive and mutilating arthritis, resulting in joint destruction. Extra-articular features include psoriasis, iritis, mouth ulcers, colitis and aortic valve disease.

There is no single blood test to diagnose psoriatic arthritis, but it is recognised that individuals affected are usually rheumatoid factor negative and do not develop rheumatoid nodules. Markers of inflammation may be elevated in active psoriatic arthritis.

The medical management of psoriatic arthritis is similar to other inflammatory arthritides (see management of RA below). Jones et al. (2003) concluded that parenteral high dose methotrexate and sulphasalazine are two medications that showed demonstrable efficacy in psoriatic arthritis. Sulphasalazine alters bowel flora, inhibits folate metabolism and is generally well tolerated. It is considered effective, particularly in treating persistent peripheral arthritis.

Rheumatoid arthritis

Rheumatoid arthritis (RA) is a complex, chronic inflammatory condition, which has both articular and extra-articular effects. It is the most common inflammatory arthropathy and has the potential to cause a significant impact on quality of life. The predominant features of the condition are pain, swelling, stiffness of joints, reduced levels of function, fatigue and anaemia.

RA is a polyarthropathy and affects both sides of the body symmetrically with a fluctuating disease pattern and episodic disease flares. It commonly affects the small joints of the hands and feet, although larger joints can also be affected. RA has a prevalence of 1% in the population. Although people of any age can be affected, the peak age range for onset is 40–60 years and it affects women more frequently: 3:1 ratio. RA has a significant impact on life and can affect roles, relationships and levels of independence as the disease progresses.

The pathophysiology of rheumatoid arthritis is not fully understood and the initial trigger is unknown. It is an autoimmune condition where pro-inflammatory cytokines are known to have an important role in the pathogenesis causing chronic inflammation. Inflammation is the body’s normal response to tissue injury, whether caused by bacteria, trauma, chemicals, heat or other phenomenon. Inflammation usually subsides when its task is completed, but maintenance of the inflammation in RA is thought to be caused by an autoimmune reaction in inflammatory arthritis. Inflammation of the synovial membrane surrounding the joint capsules and tendon sheaths is called synovitis. The synovial membrane is the inner membrane of tissue that lines a joint and secretes synovial fluid. The main function of this fluid is to lubricate the joint. It has been suggested that pathological changes caused by synovitis occur in three stages (Hill and Ryan 2000):

1. Cellular stage – joint becomes warm, swollen and tender causing stiffness and restricted movement.
2. Inflammatory stage – granulocytes accumulate in the synovial fluid before their destruction during the inflammatory process causes the release of enzymes.
3. Destructive stage – primarily affects the hyaline cartilage as vascular granulation tissue or “pannus” starts to erode the outer cartilage around the joint.

The symptoms of inflammation are redness, pain, heat, swelling and possibly loss of function of the affected joint. The clinical presentation of RA is often pain, persistent synovitis and early morning stiffness. Initial presentation is usually of symmetrical joint involvement with pain and inflammation of the metacarpal phalangeal (MCP), proximal interphalangeal (PIP) and metatarsal phalangeal (MTP) joints, although this may progress to other joints. Affected joints are often described as stiff, as if trying to move them against a resistant force. There are also extra-articular features of rheumatoid arthritis and these include fever, weight loss, fatigue, anaemia, ocular problems (scleritis, episcleritis and keratoconjunctivitis sicca), cardiac (pericarditis, endocarditis, pulmonary pleural effusions, and fibrosing alveolitis) and osteoporosis. The American College of Rheumatology (ACR) proposed in 1987 a set of classification criteria. These criteria, were initially meant for the enrolment of patients in clinical trials, but in some cases were used for diagnosis, they have shown unsatisfactory performance recently in the setting of early arthritis. In 2010 the ACR and the European League Against Rheumatism (EULAR) jointly developed new classification criteria, aiming to allow earlier patient classification, treatment and inclusion in clinical trials. The 2010 criteria include tender and swollen joint count, acute phase reactants, anti-cyclic citrullinated peptide antibodies (ACPA) or rheumatoid factor (RF) and symptom duration. These clinical and laboratory data are combined into a score ranging from 0 to 10.

NICE (2009a) recommends that people with suspected persistent synovitis are referred for specialist rheumatologist opinion with diagnosis based on clinical findings. Urgent referral should be made for patients who present with the small joints of the hands or feet affected, more than one joint affected and if there is a delay of three months or longer from the onset of symptoms.

A number of key blood tests assist in the diagnosis and monitoring of RA. These are full blood count, liver function and biochemistry tests, ESR and CRP. Immunological tests include rheumatoid factor, antinuclear antibody and anti-cyclic citrulline peptide. These are measures of autoantibodies, which are groups of immunoproteins produced by the immune system that mistakenly target and damage specific tissues and organs. Rheumatoid factor is an important immunological investigation as it determines whether RA is seropositive or seronegative. The significance of this is that seropositive RA may progress to a more aggressive form of the condition. Approximately 80% of people with RA are rheumatoid factor positive but a positive result alone does not mean a diagnosis of RA as it is thought that up to 5% of the population are rheumatoid factor positive without having rheumatoid arthritis. Anti-CCP helps to determine the prognosis of RA and is predictive of joint damage. It is a relatively new test and, therefore, not performed as a standard investigation in all centres.

X-ray remains a useful investigation for monitoring joint deterioration where bone erosions clearly appear. The use of ultrasound scanning is becoming standard practice in assessing and measuring the degree of synovitis in joints and soft tissue. It can also ascertain early erosions and tendon ruptures (Kane et al., 2004).

Management

Management of RA should include early detection and treatment to control symptoms and complications, thus delaying disease progression, but parallel to regular monitoring of drug treatments. NICE has developed a clinical guideline on the management and treatment of RA in adults (2009a). Medication is recommended to control inflammation and pain, reduce disease progression, joint damage, disability and loss of function, achieve remission and improve quality of life. Drug therapy relies on various combinations of:

• analgesics
• NSAIDs
• corticosteroids
• DMARD (disease-modifying anti-rheumatic drugs)
• biologic therapies

Analgesics are used to reduce pain with anti-inflammatories reducing pain and stiffness caused by inflammation. NSAIDs are usually taken on a regular basis with disease-modifying anti-rheumatic drugs. Corticosteroids reduce inflammation, but are associated with significant long-term side effects such as hypertension, diabetes, osteoporosis and muscle wasting and are, therefore, mainly only used to provide temporary symptom relief. These drugs can be administered orally, intra-muscularly, intra-articularly or intravenously. Disease-modifying anti-rheumatic drugs (DMARDS) are the main second line treatment for patients with RA. They are used to suppress disease activity, often in combination with first line treatments and are recommended in the early stages of RA development. They can prevent the development of erosions and deformities. There are a number of different DMARDs with different modes of action, special precautions, indications, side effects and monitoring requirements. DMARDs can be used as monotherapy or in combination. Some of these include:

• Methotrexate: 7.5 mg once weekly to a maximum dose of 25 mg weekly. This is an immunosuppressant that can slow down the progression of arthritis making significant improvement in general wellbeing. It is usually taken orally in weekly doses, but can also be given by weekly injection. It is probably the most effective of the conventional disease-modifying drugs for moderate to severe rheumatoid arthritis
• Sulphasalazine: 500 mg daily to a maximum dose of 2–3 grams daily
• Combination of antibiotic and anti-inflammatory: it is usually commenced at 500 mg daily and increased weekly to a maximum tolerated dose of 2–3 grams daily
• Leflunomide: 10–20 mg daily
• Hydroxychloroquine: initially 400 mg daily, then typically reduced to 200 mg daily. This is an antimalarial compound that has been shown to suppress the immune system in a non-specific way. A rare side effect is accumulation of the drug at the back of the eye so patients must have periodic eye tests.

The DMARDs, penicillamine (for patients allergic to penicillin) and gold (used since the 1920s) have similar actions but are less commonly selected now as the time for onset of benefit can take up to six months.

Other management options

The development of monoclonal antibodies and molecules targeted at TNF has improved the management of patients with rheumatoid arthritis, offering a therapeutic option for highly active disease, uncontrolled by traditional DMARD therapies. This option improves function and reduces pain, early morning stiffness, swollen joints and fatigue and induces and maintains remission (Anderson, 2004). There are number of biologic therapies licensed for use in RA all of which block cytokines, reducing inflammation. Anti-TNF-alpha therapies may vary in their mode of administration, indications, dosing and side effects (Table 13.2).

As RA has a considerable psychosocial impact on the patient with reports of depression, low self-esteem and isolation, a multi-disciplinary approach is recommended, including access to specialist physiotherapy, occupational therapy, podiatry and nurses (NICE 2009). Specialist physiotherapy aims to promote general fitness and exercise, as well as teaching specific exercises for joint flexibility, muscle strengthening and managing functional impairments. Hydrotherapy may be offered. This can also help to control pain and referral in the early stages of the disease can help prevent malalignment. Most patients also obtain relief from heat aids, and some using TENS.

Specialist occupational therapy facilitates independence. Problems with hand function are evaluated and appropriate management advice given. Aids to assist with daily living may include gadgets to help with washing and dressing. Specialist podiatrists provide advice with regard to footwear and foot care. The feet are often affected by RA causing mechanical damage and pain. Insoles and suitable footwear can be discussed. Specialist nurses are involved in monitoring and advising people about how to manage their disease to enable optimal physical, psychological and social functions. There are a number of specific specialist monitoring tools used by the expert nurse, for example disease activity (DA): DAS28 score alongside blood tests i.e. inflammatory markers ESR and CRP; daily function: health assessment score (HAQ); and general wellbeing: arthritis impact measurement scale. The specialist disease monitoring tools highlighted here are unlikely to be used by the orthopaedic nurse. Important facets of the role include patient education, facilitating self-management of symptoms, support at diagnosis and throughout the disease process, drug counselling and monitoring and the coordination of care within the multi-disciplinary team. The rheumatology nurse specialist can also provide telephone support and review. Nurses within the hospital environment may be familiar with caring for patients during disease flares or advising patients with regard to elective procedures.

Osteoporosis

Metabolic bone disease is the term used to describe a range of conditions inclusive of osteoporosis, Paget’s disease, osteomalacia and osteogenesis imperfecta (OI) (see Chapter 22 for further information regarding OI) that affect the quality of bone and are characterised by pain, deformity and fracture. This chapter will only discuss the most common of these; osteoporosis. The World Health Organization (WHO 1994, p. 12) define osteoporosis as

(a progressive systemic skeletal disease characterized by low bone mass and micro-architectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture.)

One in two women and one in five men over the age of 50 in the UK will fracture a bone mainly because of osteoporosis, with an estimated three million people in the UK alone suffering from the condition (www.nos.org.uk). Although fractures can occur in different parts of the body, the wrist, hip and spine are most commonly affected. Each year the numbers of people with osteoporosis in the UK rise as the population ages, resulting in over 70 000 hip fractures, 50 000 wrist fractures and 120 000 spinal fractures. Johnell and Kanis (2006) report the condition leading to nearly nine million fractures annually worldwide. Direct medical costs from fragility fractures to the UK healthcare economy were estimated at £1.8 billion in 2000, with the potential to increase to £2.2 billion by 2025, and with most of these costs relating to hip fracture care (see Chapter 18 for further exploration of fragility fractures relating to osteoporosis).

Prevention may not be totally attainable but the risk and severity can be reduced. For example, childhood through to young adulthood is the time to ‘bank’ good quality bone through diet and weight bearing activities as bone loses density with age. Consequently, as we age we are more at risk of a fragility fracture. From our mid-20s onwards our bodies constantly repair and renew bone, with whole parts of our skeletons reproduced every four to seven years. This process, known as ‘bone remodelling’, takes place on the bone’s surface thanks to two sets of cells – osteoclasts and osteoblasts. Then from around the age of 40, the osteoclasts become more active and the osteoblasts less active; so more bone is removed and less is formed. This is known as ‘age-related bone loss’ which can lead to osteoporosis, particularly for those whose bones preexist with low density. By the age of 60 approximately 15% of all women have osteoporosis and this figure increases to over 25% by the age of 80 (NICE 2008b). Because of increased bone loss after the menopause in women and age-related bone loss in both women and men, the prevalence of osteoporosis increases markedly with age:

(…because of increased bone loss after the menopause in women, and age-related bone loss in both women and men, the prevalence of osteoporosis increases markedly with age, from 2% at 50 years to more than 25% at 80 years, 52% in women. As the longevity of the population increases, so will the incidence of osteoporosis and fragility fracture.) (NICE 2012)

Education is therefore fundamental in the prevention and control of osteoporosis and in raising awareness, especially for primary and secondary prevention in post-menopausal women. The practitioner must identify what the patient knows already, identify risk factors, and inform of treatments and associated side effects of drug interventions. Box 13.1 provides examples of appropriate educational information.

Box 13.1 Patient education on osteoporosis

Diagnosis

Osteoporosis is usually diagnosed from a bone scan post-fracture or at an osteoporosis clinic. The Dual Energy X-ray Absorptiometry (DXA) scan is currently the most accurate and reliable means of assessing bone density and associated risk of fracture. It is a simple, painless procedure that routinely uses very low doses of radiation to scan the spine/hips, wrist or heel using T and Z scores as markers (Tanna 2009). The WHO (1994) define criteria generated the T score to imply the number of standard deviations (SD) which separate the patient from the mean value of a healthy young population. A Z score is the number of SD which separate the patient from an age-matched health population. In reality, osteopenia (bone mineral density lower than normal) has a T score between –1 and –2.5 SD, with osteoporosis a T score of –2.5 SD or below and progressively more severe osteoporosis; a T score of –2.5 SD or below with one or more associated fractures.

Drug treatments

Bisphosphonates are non-hormonal drugs that help maintain bone strength and reduce fracture rates. They inhibit osteoclast action and slow down the rate of bone resorption to maintain the patient’s current bone mineral density (BMD) level and reduce the risk of fracture. The drugs have poor rates of absorption and potential gastrointestinal side effects and compliance is reported to be poor. Guidance on taking the drug is fundamental to patient compliance and outcome; it should be swallowed on an empty stomach, with a glass of water, while standing, then to remain upright and fasting for 30 minutes. The main drugs in this range are alendronic acid or alendronate (Fosamax), cyclical etidronate (Didronel PMO), ibandronate (Bonviva), risedronate (Actonel) and zoledronic acid (Aclasta). These have been shown to reduce the risk of fractures in the spine and, in some cases, the hip. NICE (2012) recommend Alendronate as a treatment option for the primary prevention of osteoporotic fragility fractures in the following groups:

• Women aged 70 years or older who have an independent clinical risk factor for fracture or an indicator of low BMD and who are confirmed to have osteoporosis. In women aged 75 years or older who have two or more independent clinical risk factors for fracture or indicators of low BMD. A DXA scan may not be required if the responsible clinician considers it to be clinically inappropriate or unfeasible.
• Women aged 65–69 years who have an independent clinical risk factor for fracture and who are confirmed to have osteoporosis.
• Postmenopausal women younger than 65 years who have an independent clinical risk factor for fracture (see below) and at least one additional indicator of low BMD and who are confirmed to have osteoporosis.
• When the decision has been made to initiate treatment with Alendronate, the preparation prescribed should be chosen on the basis of the lowest acquisition cost available.

Alternative therapies include:

• Hormone replacement therapy (HRT) – oestrogen replacement for women at the menopause stage of their life, which helps maintain bone strength and reduces fracture rates.
• Selective oestrogen receptor modulators (SERMs) drugs act in a similar way to oestrogen on the bone, helping to maintain bone strength and reduce fracture rates, especially in the spine.
• Testosterone therapy is testosterone replacement for men with low testosterone levels to help maintain bone strength, calcium and vitamin D.

Osteomyelitis

Osteomyelitis is an acute or chronic infection of bone and its structures. The most common organism responsible is staphylococcus aureus (Lew and Waldvogel 2004). It is a progressive condition and associated inflammation leads to necrotic destruction of bone that can lead to an acute infection becoming chronic. It is relatively uncommon because bone is resistant to infection so it tends to occur in patients with significant risk factors such as diabetes that reduce their resistance or make their bone more vulnerable through trauma or surgery. Its severity and progression can depend on the source of infection, the virulence of the organism involved and the general health of the patient (Brady et al., 2006). It is often a devastating problem for patients as it is very difficult to treat because of necrosis and disruption to blood supply to bone which means that systemic and local antibiotic therapy is unsuccessful. Many years of pain and disability are often the result sometimes with suppurating sinus wounds. The prevention of osteomyelitis following injury and surgery is a major driver for good infection prevention and control practice throughout the patient’s care journey. It is also one of the reasons that prophylactic antibiotic therapy is often given following open fracture and orthopaedic surgery. Gosselin et al. (2009) found antibiotics to reduce the incidence of early infections in open fractures of the limbs.

There are several different classifications of osteomyelitis depending on the source of infection:

Endogenous (haematogenous) osteomyelitis

occurs when pathogens are carried in the blood from sites of infection elsewhere in the body – a process sometimes known as remote ‘seeding’. The infection spreads from bone to adjacent soft tissues or remote infections such as urinary tract infection. The prevention of such infections is, therefore, central to orthopaedic care. This includes, for example, the avoidance of urinary catheterisation.

Endogenous osteomyelitis is more common in infants, children and older people. Before puberty bacteria can gain access to a child’s bone, often accumulating in the metaphyseal region (growth area of the bone). The bacteria proliferate and trigger an initial inflammatory response. Once inflammation is initiated the small vessels in bone thrombose. The build-up of pressure in the bone causes the inflammatory exudate to move to the bone cortex separating the periosteum from underlying bone and resulting in a painful subperiosteal abscess. The white cells cannot remove the infected material, resulting in accumulation of infected and ischaemic tissue and the eventual necrosis of underlying bone tissue (sequestrum) which is radiologically visible. Lifting of the periosteum also stimulates an intense osteoblastic response and new bone is laid down partially or completely surrounding the infected bone (involucrum). Openings in the involucrum allow the exudate to escape into surrounding tissues and ultimately the skin through a sinus tract.

Exogenous osteomyelitis

is a key route of transmission; the infection enters through open fractures, penetrating wounds and surgical procedures.

Acute osteomyelitis in adults (sudden onset)

is usually haematogenous in origin but may be due to trauma in the femur, tibia humerus and thoracolumbar spine. Spinal osteomyelitis is more common in adults past middle age and can result in a spinal cord compression. Clinical presentation often includes (Chihara and Segreti 2010):

• a history of injury 2–3 months previously
• abrupt onset of high pyrexia
• generally feeling unwell
• restriction of movement of affected bone
• pain and tenderness including on-bone palpation
• local signs of inflammation including swelling, redness, heat and localised pain.

It is important that the symptoms are not confused with cellulitis, acute septic arthritis, acute rheumatism or a sickle cell crisis.

Investigations include:

• history and clinical examination
• blood counts
• microbiological culture of blood, wound swabs
• aspiration of material from the site of infection for microbiological analysis
• X-ray
• bone scan/CT/MRI.

Imaging will show soft-tissue swelling, narrowing or widening of joint spaces, bone destruction, and periosteal reaction. Bone destruction, however, is not apparent until after 10–21 days of infection (Lew and Waldvogel 2004).

Treatment options

include measures to support the limb or spine with a view to reducing pain. This might include traction, splintage or application of a cast. Intravenous antibiotic therapy is used initially and to cover any surgical period up to two weeks post-surgery. The switch to oral therapy may happen once the clinical condition stabilises and microbiology results suggest infection is resolved. Treatment for acute infection is usually for 4–6 weeks. Chronic infection is considered below. High doses of antibiotics are required to achieve suitable bone penetration in high enough concentrations in necrotic avascular bone (Lew and Waldgovel 2004)

Chronic osteomyelitis (slower onset)

is a severe, persistent and sometimes incapacitating infection of bone and bone marrow which is on the increase due to predisposing conditions such as diabetes mellitus and peripheral vascular disease (Hatzenbuehler and Pulling 2011). Aetiology includes inadequately treated acute osteomyelitis, post open fracture or surgery, infection with TB and syphilis, joint replacement/internal fixation of open fractures and contiguous spread from soft tissue infection. The inflammatory reaction to infection in bone continues over time, leading to sclerosis and deformity with presence of sequestrum, involucrum, local bone loss and persistent drainage and/or sinus tract formation. The most common organisms are staph. aureus, streptococci, pneumococci and myobacterium tuberculosis (Kneale and Davis 2005). Clinical presentation includes:

• previous history of acute infection/osteomyelitis
• chronic bone pain
• sinus formation and purulent drainage
• low grade or absent pyrexia
• if a sinus tract becomes obstructed the patient can present with a localised abscess, soft tissue infection or both
• persistently feeling unwell.

Treatment includes antibiotic therapy (IV/Oral) for a minimum of 6–12 weeks. Surgery is almost always necessary with chronic osteomyelitis as necrotic and dead bone needs to be debrided. Management might also include ‘Papineau technique’/vacuum assisted closure (VAC) (Archdeacon and Messerschmitt 2006) with flaps, antibiotic impregnated beads, bone grafting, soft tissue management and stabilisation. This may often involve the removal of previous metalwork and instability caused by bone damage or loss may require external fixation. Prognosis is dependent on the patient’s general health status. Outcomes are improved if treatment is started 3–5 days after the onset of the infection.

Timely diagnosis and intervention in an otherwise well patient can lead to full recovery, although follow-up over several months is needed to monitor for relapse. The condition can have a psychological impact on the patient if recovery is slow and pain severe.

Back pain

Back pain is a complex series of conditions with considerable variability in pathology and outcome. Most patients with new episodes recover within a few weeks but recurrence is common and individuals with chronic, long-standing back pain tend to show a more persistent course. Most back pain, fortunately, responds to a set of non-surgical interventions that facilitate a gradual return to normal activity for the patient. Patients need to be encouraged to move despite the presence of pain to aid recovery. Progressively intense range of movement and strengthening exercises offer improved stability of the lumbar spine under the guidance of a physiotherapist, while drugs facilitate increased movement and recommencement of normal activities. Drug regimens may include simple analgesics, NSAIDs and muscle relaxants, which can hasten a return to function. When back pain becomes chronic additional health professionals may become involved. The chronic pain service is often pivotal in developing a personalised plan with a variety of approaches to manage the differing types of pain, e.g. stronger opioids for escalating nociceptive type pain, additional medication for neuropathic pain and acupuncture, whilst psychology may better support a reduction in patient’s mood /depression with antidepressants and alternative interventions such as cognitive behavioural therapy as chronic pain does appear to increase the risk of depression in some patients.

Low back pain (LBP) is the most common condition within the spectrum with many people experiencing it at some point in their life. Most low back pain episodes are mild and rarely disabling, with only a small proportion of individuals seeking intervention. LBP can impact upon the person’s quality of life due to reduced mobility and pain and differential diagnosis is desirable to establish a probable cause, diagnosis and suitable treatments. A general practitioner (GP) most often makes the referral to an orthopaedic consultant which leads to a more in-depth history taking and physical examination using the ‘look, feel and move’ in conjunction with radiological evidence e.g. X-ray, MRI and CT in an attempt to ascertain a diagnosis which is not always attainable. ‘Listening’ to the patient and family gives the practitioner the best opportunity to find the cause of low back pain. Treatment and care needs to consider the patients’ individual needs and preferences. Good communication the provision of information is central in facilitating patient involvement in their care. NICE (2009b) offers specific guidance for the early management of low back pain and these are summarised in Box 13.2.

Box 13.2  Evidence digest. Reproduced with permission from NICE

Scoliosis

The spine has gentle curves that develop as a child grows, but within such natural curves three key deformities can develop; scoliosis, kyphosis and lordosis. Only scoliosis, the type most commonly met by the practitioner, will be discussed here. Scoliosis refers to a side-to-side curvature of the spine that affects a small percentage of the population, approximately 2% in women and less than half a percent of men. The condition has familial tendencies and the majority of scoliosis is ‘idiopathic’, (of no known cause) usually starting in the early teens or pre-teens and gradually progressing in severity of the curvature as growth occurs. Once the rapid growth of puberty is over, mild curves often do not change whilst severe curves nearly always develop further. Although scoliosis can occur in children with cerebral palsy, muscular dystrophy, spina bifida and other miscellaneous conditions, most scoliosis is found in otherwise healthy young people. Therefore, parents should watch for the following ‘signs’ of scoliosis beginning when their child is about eight years of age, with any one sign warranting investigation:

• uneven shoulders
• prominent shoulder blade or shoulder blades
• uneven waist
• elevated hips
• leaning to one side.

Adult scoliosis may represent the progression of a condition that began in childhood and was not diagnosed or treated during growth. What might have started out as a slight or moderate curve could have progressed in the absence of treatment. If allowed to progress, in severe cases adult scoliosis can lead to chronic severe back pain, deformity, and difficulty in breathing.

Cobb’s angle is the measurement used for the evaluation of curves in scoliosis on an AP radiographic image of the spine using a protractor. A line is drawn along the superior end plate of the superior end vertebra involved in the curve and a second line drawn along the inferior end plate of the inferior end vertebra. If the end plates are indistinct, the line may be drawn through the pedicles. The angle between these two lines (or lines drawn perpendicular to them) is measured as the Cobb angle. Shaw et al. (2012) reported upon the use of smart phone technology to offer an equivalent Cobb measurement tool equal to the manual protractor. In S-shaped scoliosis, where there are two contiguous curves, the lower end vertebra of the upper curve will represent the upper end vertebra of the lower curve. Because the Cobb angle reflects curvature only in a single plane and fails to account for vertebral rotation it may not accurately demonstrate the severity of three dimensional spinal deformities. As a general rule a Cobb angle of 10 is regarded as a minimum angulation to define scoliosis.

Treatment options include:

• Doing nothing, which may be reasonable depending on the age of the person and the predicted outcome. Doing nothing in the teen years though may be disastrous.
• Bracing has been shown to be an effective method to prevent curves from getting more progressive. However this treatment is reserved for children and young people in whom a rapid increase in the curve needs to be thwarted. A brace worn 16 or more hours per day has been shown to be effective in preventing 90% or more of the curves from getting worse. Unfortunately, a brace worn 23 hours per day and worn properly does not guarantee that the curve will not continue to increase. Yet, in curves that are mild i.e. between 20 and 35 degrees, a brace may be quite effective. However, bracing cannot “hold” curves greater than 40 degrees. The brace may feel hot, hard and uncomfortable while it normally can’t be seen under the clothes and can make a young person more self-conscious about their body image (http://www.scoliosisrx.com/).
• For those who already have a significant curve and deformity, surgery can reduce the curve and significantly reduce the deformity.

Surgery is usually offered to teen and pre-teens who already have a curve of around 40 degrees or more. Surgery can commence around 40 degrees while there are many excellent surgeons who defer to 45 or 50 degrees. In the adult the reasons for surgery include increasing discomfort or pain with an increasing curve. For many women the combination of a deformity in the hip line and the increasing discomfort make surgery a reasonable option. Others note the increasing deformity in the chest coupled with an increase in the rib hump. However for those persons surgery can (not always and certainly not guaranteed) reduce the deformity and the discomfort or pain.

Common surgical intervention includes anterior and posterior spinal fusion. Posterior spinal infusion only (Matusz et al., 2005) with posterior spinal fusion (PSF) with spinal instrumentation has been the mainstay of surgical treatment since the late 1960s. Thoracoscopic anterior instrumentation is an alternative as instead of a long open thoracotomy to obtain exposure of the anterior spine, small incisions are made to allow introduction of a thoracoscope and working instruments. The advantages are less post-operative pain in the chest wall, better long-term cosmetics and equal release when compared to open discectomy plus alternative growth rod instrumentation (Ember and Noordeen 2005).

Spinal stenosis

Spinal stenosis refers to narrowing of the central spinal canal. Although narrowing does not always result in nerve compression, it can create pressure on the nerves, often resulting in pain or numbness in the region impacted by the compressed nerve or nerves. There are many causes including tumours, congenital defects, physical injury and bone disease. However the most prevalent causes are the ageing effects of intervertebral disc degeneration, bone overgrowth and ligament thickening. Lumbar and cervical areas are most commonly affected and both lead to significant pain, disability and impact on quality of life. Lumbar spinal stenosis has become the most common indication for spinal decompression surgery in older patients.

Intervertebral disc disease

Age-related changes in the intervertebral disc can lead to degeneration and increased likelihood of a clinical problem. A prolapsed intervertebral disc (often termed ‘slipped disc’) commonly occurs in the lumbar and cervical areas which have more mobility which puts the discs at high risk of damage (Smith 2005). The primary symptom is pain of varying severity and frequency. Depending on the site of the disc prolapse and the nerve involvement, the patient will typically have intense radicular (nerve root) pain. The pressure that the disc puts on the nerve roots often causes neurological symptoms in addition to the pain, with some patients developing motor weakness.

The management of back pain is usually treated conservatively initially with MDT involvement and discussion with patients regarding realistic options (Murray, 2011). Medication, exercises and/or a local steroid injection via epidural may benefit patients. Surgery is indicated if the following indicators are present:

• unrelenting leg pain
• neural damage
• cauda equina syndrome

A central disc prolapse constitutes a medical emergency however. An immediate MRI scan is required. Decompression within 24 hours of the onset of symptoms is needed as the disc presses on the cauda equina, causing the following motor and sensory problems:

• loss of perianal sensation known as ‘saddle anaesthesia’
• bilateral motor weakness in the legs
• sphincter disturbance to the bowel and bladder.

Summary

All key orthopaedic conditions discussed here continue to challenge patients and the nurse practitioners who care for them. With significant development of professional roles and increasing autonomy for nurses along with heightened engagement in evidence based practice and national guidance such as that from NICE the way in which care is delivered can ensure optimum outcomes whether treatment is conservative, pharmacological or surgical.

Recommended further reading

1. Brady, R.A., Leid, J.G., Costerton, J.W. and Shirtliff, M.E. (2006) Osteomyelitis: clinical overview and mechanisms of infection. Clinical Microbiology Newsletter, 28(9), 65–72.
2. Hatzenbuehler, J. and Pulling, T.J. (2011) Diagnosis and management of osteomyelitis. American Family Physician, 1:84 (9),1027–1033.
3. Murray, M.M. (2011) Reflections on the development of nurse-led back pain triage clinics in the UK. International Journal of Orthopaedic and Trauma Nursing, 15(3), 113–120.
4. National Institute for Clinical Evidence (NICE) (2009a) Rheumatoid Arthritis – Full Guideline Rheumatoid Arthritis: National Clinical Guideline for Management and Treatment in Adults. NICE, London.
5. Tanna, N. (2009) Osteoporosis and fragility fractures: identifying those at risk and raising public awareness. Nursing Times, 105(38), 28–31.

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