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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2826_Библиотеки_им_академика_М_И_Перельмана.pdf
Back Pain 273
BACK PAIN
Lumbar back pain
Lumbar back pain is a common symptom experienced by most people
at some time in their lives. Only a few patients have a serious underlying
disorder. Mechanical back pain is a common cause in young people. It starts
suddenly, is often unilateral, and may be helped by rest. It may arise from
the facet joints, spinal ligaments or muscle. The history, physical examination
and simple investigations will also often identify the minority of patients with
other causes of back pain (Table 7.3).
The age of the patient helps in deciding the aetiology of back pain
because certain causes are more common in particular age groups. These
are illustrated in Table 7.4.
Table 7.3 Causes of lumbar back pain
Causes History and examination
Mechanical Lumbar disc prolapse
Inflammatory
Serious causes
Others
*Indicates the ‘red flags’ in a patient with lumbar back pain. Onset of thoracic pain is also
a ‘red flag’.
HIV, human immunodeficiency virus; TB, tuberculosis.
Osteoarthritis
Fractures
Spondylolisthesis
Spiral stenosis
Ankylosing spondylitis
Infection (see below)
Metastases
Multiple myeloma
Tuberculosis
Osteomyelitis
Bacterial osteomyelitis
Spinal and root canal
stenosis
Osteomalaci HIV, human immunodeficiency virus; TB,
tuberculosis. a, Paget’s disease, referred pain from pelvic
abdominal disease
Often sudden onset
Pain worse in the evening
Morning stiffness is absent
Exercise aggravates pain
Gradual onset
Pain worse in the morning
Morning stiffness is present
Exercise relieves pain
Age <20 or >50 years*
Constant pain without relief*
History of TB, HIV, carcinoma,
steroid use*
Systemically unwell: fever,
weight loss*
Localized bone tenderness*
Bilateral signs in the legs*
Neurological deficit involving
more than one root level*
Bladder, bowel or sexual
function deficits*
274 Rheumatology
Table 7.4 Low back pain – disorders most commonly found in
specific age groups
15–30 years 30–50 years 50 years and over
Mechanical Mechanical Degenerative joint
Prolapsed intervertebral
disc
Ankylosing spondylitis
Spondylolisthesis
Fractures (all ages)
Infective lesions (all ages)
Prolapsed intervertebral
disc
Degenerative joint disease
Malignancy
Fractures (all ages)
Infective lesions (all ages)
disease
Osteoporosis
Paget’s disease
Malignancy
Myeloma
Fractures (all ages)
Infective lesions
(all ages)
Investigations
A detailed history and physical examination (see Table 7.3) will lead to the
diagnosis in many cases. The key points are age, speed of onset, the presence of motor or sensory symptoms, involvement of the bladder or bowel, the
presence of stiffness and the effect of exercise. Young adults with a history
suggestive of mechanical back pain and with no physical signs do not need
further investigation.
• Full blood count, ESR and serum biochemistry (calcium, phosphate,
alkaline phosphatase) are required only when the pain is likely to be
dueto malignancy, infection or a metabolic cause. Prostate-specific
antigen (PSA) should be measured if secondary prostatic disease is
suspected.
• Spinal X-rays are only indicated if there are ‘red flag’ symptoms and
signs (Table 7.4) which indicate a high risk of more serious underlying
pathology.
• Bone scans (p. 270) show increased uptake with infection or
malignancy.
• MRI is useful when neurological symptoms and signs are present. It is
useful for the detection of disc and cord lesions. Computed tomography
(CT) scans demonstrate bone pathology more effectively.
Management
The treatment depends on the cause. Mechanical back pain is managed
with analgesia, rest and physiotherapy. Patients should stay active within the
limits of their pain. Exercise programmes reduce long-term problems.
Intervertebral Disc Disease 275
INTERVERTEBRAL DISC DISEASE
Acute disc disease
Prolapse of an intervertebral disc results in acute back pain (lumbago),
with or without radiation of the pain to areas supplied by the sciatic
nerve (sciatica). It is a disease of younger people (20–40 years) because
the disc degenerates with age and in elderly people is no longer capable
of prolapse. In older patients, sciatica is more likely to be the result of
compression of the nerve root by osteophytes in the lateral recess of the
spinal canal.
Clinical features
There is a sudden onset of severe back pain, often following a strenuous
activity. The pain is often clearly related to position and is aggravated by
movement. Muscle spasm leads to a sideways tilt when standing. The
radiation of the pain and the clinical examination findings depend on the
disc affected (Table 7.5), the lowest three discs being those most commonly
affected.
Investigations
Investigations are of very limited value in acute disc disease and X-rays are
often normal. MRI is usually reserved for patients in whom surgery is being
considered (see later).
Management
Treatment is aimed at the relief of symptoms and has little effect on the
duration of the disease. In the acute stage, treatment consists of bed rest on
a firm mattress, analgesia and occasionally epidural corticosteroid injection
in severe disease. Surgery is only considered for severe or increasing neurological impairment, e.g. foot drop or bladder symptoms. Physiotherapy is
used in the recovery phase, helping to correct posture and restore movement.
Chronic disc disease
Chronic lower back pain is associated with ‘degenerative’ changes in the
lower lumbar discs and facet joints. Pain is usually of the mechanical type
(see above). Sciatic radiation may occur with pain in the buttocks radiating
into the posterior thigh. Usually the pain is long-standing and the prospects
for cure are limited. However, measures that have been found useful include
NSAIDs, physiotherapy and weight reduction. Surgery can be considered
when pain arises from a single identifiable level and has failed to respond to
conservative measures, and fusion at this level, with decompression of the
affected nerve roots, can be successful.
276 Rheumatology
Table 7.5 Symptoms and signs of common root compression
syndromes produced by lumbar disc prolapse
Root
Pain Sensory loss Motor
lesion
S1
L5
L4
From buttock
down back of
thigh and leg
to ankle and
foot
From buttock
to lateral
aspect of leg
and dorsum
of foot
Lateral aspect
of thigh to
medial side
of calf
Sole of foot
and posterior
calf
Dorsum of
foot and
anterolateral
aspect of
lower leg
Medial aspect
of calf and
shin
weakness
Plantar flexion
of ankle and
toes
Dorsiflexion of
foot and toes
Dorsiflexion
and inversion
of ankle;
extension of
knee
Reflex
lost
Ankle
jerk
None
Knee
jerk
Other
signs
Diminished
straight leg
raising
Diminished
straight leg
raising
Positive
femoral
stretch test
Mechanical problems
Spondylolisthesis
Spondylolisthesis is characterized by a slipping forward of one vertebra on
another, most commonly at L4/L5. It arises because of a defect in the pars
interarticularis of the vertebra, and may be either congenital or acquired
(e.g. trauma). The condition is associated with mechanical pain which
worsens throughout the day. The pain may radiate to one or other leg and
there may be signs of nerve root irritation. Small spondylolistheses, often
associated with degenerative disease of the lumbar spine, may be treated
conservatively with simple analgesics. A large spondylolisthesis causing
severe symptoms should be treated with spinal fusion.
Spinal stenosis
Narrowing of the lower spinal canal compresses the cauda equina, resulting in back and buttock pain, typically coming on after a period of walking
and easing with rest. Accordingly, it is sometimes called spinal claudication.
Possible aetiologies include disc prolapse, degenerative osteophyte formation, tumour and congenital narrowing of the spinal canal. CT and MRI will
demonstrate the cord compression and treatment is by surgical decompression. Rest helps, as does bending forwards, a manoeuvre that opens the
spinal canal.
Osteoarthritis 277
Neck pain
Disc disease may occur in the neck as well as in the lumbar spine. This may
be either acute or chronic, the latter in association with osteoarthritis. The
three lowest cervical discs are most often affected, and there is pain and
stiffness of the neck with or without root pain radiating to the arm. Chronic
cervical disc disease is known as cervical spondylosis.
OSTEOARTHRITIS
Osteoarthritis (OA) is a disease of synovial joints (see Fig. 7.1) and is the most
common form of arthritis.
Epidemiology
The prevalence of OA increases with age, and most people over 60 years
will have some radiological evidence of it although only a proportion of these
have symptoms. OA occurs worldwide, it is more common in women, and
there is a familial tendency to develop nodal and generalized OA. Other risk
factors are obesity, a fracture through a joint, congenital joint dysplasias, preexisting joint damage of any cause, occupation (e.g. OA of the hip in farmers
and labourers) and repetitive use and injury associated with some sports.
Pathology and pathogenesis
OA is the result of an active process around the whole joint with alterations in
subchondral bone, ligaments, capsule, synovial membrane as well as articular
cartilage. Rather than simply the inevitable result of trauma and ageing, OA
reflects an active process, which is sometimes inflammatory, characterized by
progressive destruction and loss of articular cartilage with an accompanying periarticular bone response. The exposed subchondral bone becomes sclerotic, with
increased vascularity and cyst formation. Attempts at repair produce cartilaginous
growths at the margins of the joint which later become calcified (osteophytes).
Several mechanisms have been proposed:
• Abnormal stress and loading, leading to mechanical cartilage damage.
• Obesity is a risk factor for developing OA of the hand and knee and
thought to trigger metabolic inflammation via pro-inflammatory cytokines
that cause cartilage and bone damage.
• Metalloproteinases, e.g. stromelysin and collagenase, secreted by
chondrocytes degrade collagen and proteoglycans.
• Inflammatory mediator release (e.g. interleukin (IL)-1 and tumour
necrosis factor (TNF)-α) stimulate metalloproteinase production and
inhibit collagen production.
• Growth factors, such as insulin-like growth factor (IGF-1) and
transforming growth factor beta (TGF-β), are involved in matrix repair
and their deficiency may impair this process. Paradoxically, increased
TGF-β may also cause increased subchondral bone density.
278 Rheumatology
• Osteoprotegerin (OPG), receptor activator of nuclear factor-κB (RANK) and
RANK ligand (RANKL) control subchondral bone remodelling. Their levels
are significantly different in OA chondrocytes. Inhibiting RANKL may
prove a new therapeutic approach in OA.
• Genetic susceptibility (35%–65% influence) from multiple genes rather
than a single gene defect. Mutations in the gene for type II collagen have
been associated with early polyarticular OA. Polymorphisms in the gene for
human aggrecan have been correlated with OA of the hand in older men.
• An inverse relationship exists between the risk of developing OA and
osteoporosis in Caucasians.
• In women, weight-bearing sports produce a two- to threefold increase in
risk of OA of the hip and knee. In men, there is an association between
hip OA and certain occupations: farming and labouring. OA may flare
after the female menopause or after cessation of hormone replacement
therapy.
Most OA is primary, with no obvious predisposing factor. Secondary OA
occurs in joints that have been damaged in some way or are congenitally
abnormal.
Clinical features
Joint pain is the main symptom, exacerbated by movement and relieved by
rest. Stiffness occurs after rest (‘gelling’) and in contrast to inflammatory
arthritis there is only transient (<30 minutes) morning stiffness. The joints
most commonly involved are the distal interphalangeal joints (DIPJs) and
first carpometacarpal joint of the hands, first metatarsophalangeal joint of
the foot and the weight-bearing joints – vertebrae, hips and knees. Elbows,
wrists and ankles are rarely affected. On examination there is deformity and
bony enlargement of the joints, limited joint movement and muscle wasting
of surrounding muscle groups. Crepitus (grating) is a common finding and is
probably due to the disruption of the normally smooth articulating surfaces
of the joints. There may be a joint effusion. Heberden’s nodes are bony swellings at the DIPJs. Bouchard’s nodes are similar but occur at the proximal
interphalangeal joints (PIPJs) (Fig. 7.2).
Differential diagnosis
OA is differentiated from RA by the pattern of joint involvement and the absence
of the systemic features and marked early-morning stiffness that occur in RA.
A chronic arthropathy (pseudo-OA) occurs, predominantly in elderly women
with severe chondrocalcinosis (p. 294) but the wrists and shoulder are usually
involved and the hands rarely involved. Chronic tophaceous gout (p. 291) and
psoriatic arthritis affecting the DIPJs (p. 289) may mimic OA.
Investigations
• Full blood count and ESR are normal. Rheumatoid factor is negative, but
positive low-titre tests may occur incidentally in elderly people.
Osteoarthritis 279
Fig. 7.2 Severe nodal osteoarthritis (OA). The distal interphalangeal joints
(DIPJs) demonstrate Heberden’s nodes (arrows). The middle finger DIPJ is
deformed and unstable. The thumb is adducted and the bony swelling of the first
carpometacarpal joint is clearly shown – ‘the squared hand of nodal OA’.
• X-rays are only abnormal in advanced disease and show narrowing
of the joint space (resulting from loss of cartilage), osteophytes,
subchondral sclerosis and cyst formation.
• MRI demonstrates early cartilage changes. It is not necessary for most
patients with suggestive symptoms and typical plain X-ray features.
Management
Treatment should focus on symptoms and functionality, not the radiological
appearances. Patient education about the disease, non-pharmacological
measures, drugs and surgery all have a role. Obese patients should be
encouraged to lose weight, particularly if weight-bearing joints are affected.
• Physical measures are the keystone of OA treatment. Local strengthening
and aerobic exercises improve muscle strength, mobility of weightbearing joints and overall aerobic fitness. Local heat or ice packs applied
280 Rheumatology
to an affected joint may help. Bracing devices, joint supports, insoles for
joint instability and footwear with shock-absorbing properties for lower
limb OA are also used. A walking stick held on the contralateral side to
the affected lower limb joint is useful. Acupuncture may also be of benefit.
• Medication. Topical, oral and injectable therapies are available and
potential benefit must be balanced against the risk of any adverse
effects, especially in the elderly. NSAIDs (p. 315), either orally or topically,
are considered first line after randomized trial data demonstrated
paracetamol to be no more effective than placebo for back pain, with
only a small benefit for hip and knee pain. NSAIDs should be used
in short courses rather than on a continuous basis. Intra-articular
corticosteroid injections produce short-term improvement when there is
a painful joint effusion; systemic corticosteroids are not used.
• Surgery. Total hip and knee replacement has transformed the
management of severe symptomatic OA. There is reduced pain
and stiffness and an associated increase in function and mobility.
Complication rates are low with loosening and late bone infection being
the most serious.
INFLAMMATORY ARTHRITIS
Inflammatory arthritis includes a large number of arthritic conditions in
which the predominant feature is synovial inflammation. The three main
subgroups of inflammatory arthritis are RA, spondyloarthritis and crystal
arthritis. There is joint pain and stiffness after rest and in the morning.
Morning stiffness may last several hours (cf. osteoarthritis). Blood tests
often show a normochromic, normocytic anaemia and raised inflammatory
markers (ESR and CRP).
Rheumatoid arthritis
RA is a chronic systemic autoimmune disorder causing a symmetrical
polyarthritis.
Epidemiology
RA affects 0.5%–1% of the population worldwide, with a peak prevalence
between the ages of 30 and 50 years.
Aetiology and pathogenesis
Genetic and environmental factors play an aetiological role.
• Sex. Women before the menopause are affected three times more
often than men, with an equal sex incidence thereafter suggesting an
aetiological role for sex hormones.
• Familial. There is an increased incidence in those with a family history
ofRA.
Inflammatory Arthritis 281
• Genetic factors. Human leucocyte antigen (HLA)-DR4 and HLA-DRB1*04
confer susceptibility to RA and are associated with development of more
severe erosive disease. Protein tyrosine phosphatase N22 (PTPN22),
STAT4 and PADI-4 have also been identified as susceptibility genes.
• Smoking is an environmental risk factor for seropositive RA.
The triggering antigen in RA is not known but factors produced by
activated T cells (interferon, IL-2 and IL-4), macrophages (IL-1, IL-8, TNF-α,
macrophage inflammatory protein), mast cells (histamine and TNF-α) and
fibroblasts (IL-6, vascular cell adhesion molecule, delay accelerating factor)
contribute to the ongoing synovial inflammation. Local production of rheumatoid factor (autoantibodies directed against the Fc portion of immunoglobulin
(Ig)) by B cells and formation of immune complexes with complement activation also maintain the chronic inflammation.
Pathology
RA is characterized by synovitis (inflammation of the synovial lining of
joints, tendon sheaths or bursae) with thickening of the synovial lining and
infiltration by inflammatory cells. Generation of new synovial blood vessels
is induced by angiogenic cytokines, and activated endothelial cells produce
adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1),
which expedite extravasation of leucocytes into the synovium. The synovium
proliferates and grows out over the surface of cartilage, producing a tumourlike mass called ‘pannus’. Pannus destroys the articular cartilage and
subchondral bone, producing bony erosions. This early damage justifies the
use of disease-modifying drugs within 3 months of onset of the arthritis to
try and induce disease remission.
Clinical features
The typical presentation is with an insidious onset of pain, early-morning
stiffness (lasting more than 30 minutes) and symmetrical swelling of the
proximal small joints of the hands and feet. There is spindling of the fingers
caused by swelling of the PIPJs but not DIPJs. The metacarpophalangeal and
wrist joints are also swollen. As the disease progresses there is weakening
of joint capsules, causing joint instability, subluxation (partial dislocation) and
deformity. The characteristic deformities of the rheumatoid hand are shown
in Fig. 7.3. Most patients eventually have many joints involved, including the
wrists, elbows, shoulders, cervical spine, knees, ankles and feet. The dorsal
and lumbar spine are not involved. Joint effusions and wasting of muscles
around the affected joints are early features. Less common presentations are
‘explosive’ (sudden onset of widespread arthritis), palindromic (relapsing and
remitting monoarthritis of different large joints) or with a systemic illness with
few joint symptoms initially.
In patients presenting with disproportionate involvement of a single joint,
septic arthritis (p. 294) must be excluded before the symptoms are attributed
to a disease flare-up.
282 Rheumatology
Swelling of MCP
and PIPJs
Z-shaped
thumb
Fig. 7.3 Characteristic hand deformities in rheumatoid arthritis. MCP,
metacarpophalanges; PIPJs, proximal interphalangeal joints.
Non-articular manifestations
Periarticular features of RA include bursitis, tenosynovitis, muscle wasting
and subcutaneous nodules known as rheumatoid nodules, which usually
occur over pressure points at the elbow, the finger joints and Achilles tendon
but may also occur in the pleura, pericardium and lung.
Other non-articular manifestations are summarized in Table 7.6. Patients
with RA also have a greater risk of infection and osteoporosis. The chronic
inflammation and endothelial damage associated with RA contributes to
accelerated atherosclerosis, which is partly responsible for the increased
mortality rate in severe RA.
Investigations
The diagnosis of RA cannot be established by a single laboratory test and
depends on the aggregation of characteristic clinical features (symmetrical
peripheral polyarthritis with morning stiffness and nodules in some patients),
blood tests and radiological appearances.
• Blood count. There is usually a normochromic, normocytic anaemia and
thrombocytosis. The ESR and CRP are raised in proportion to the activity
of the inflammatory process.
• Serum autoantibodies. Rheumatoid factor is positive in 70% of cases and
antinuclear factor at low titre in 30% (p. 270). Rheumatoid factor is not
specific for RA and may occur in connective tissue diseases and some
infections. In contrast, anti-citrullinated peptide antibodies (ACPA) (p. 270)
have high specificity (90%) and sensitivity (80%) for RA and are particularly