Osteomyelitis

Osteomyelitis

Osteomyelitis
Osteomyelitis refers to an infection of the bone marrow that can spread to the bone cortex and periosteum via the Haversian canals, resulting in inflammatory destruction of the bone; necrosis can also occur. When dead bone becomes detached from healthy bone, it is known as a sequestrum (this represents devascularization of a portion of bone, with necrosis and resorption of surrounding bone, leaving a ‘floating’ piece, and acts as a reservoir for infection as being avascular it is not penetrated by antibiotics); any bone may be affected. Bone is usually resistant to bacterial colonization; however, trauma, surgery, presence of foreign bodies or prostheses may disrupt bony integrity and lead to the onset of bone infection. Osteomyelitis may be acute or chronic (evolving over months or even years).
Osteomyelitis can be further categorized into two subgroups: haematogenous osteomyelitis is an infection resulting from haematological bacterial seeding from a remote source. Haematogenous osteomyelitis is also seen in those with distant foci of infection, for example those with urinary catheter infection. Direct (contiguous) osteomyelitis occurs where there is direct contact of infected tissue with bone; this can happen during a surgical procedure or after trauma. Clinical signs are more localized and there are often multiple organisms involved.

Pathophysiology
Bone is highly resistant to infection. Osteomyelitis only arises when there is a large organism inoculation, trauma leading to bone damage or the presence of foreign material. The pathogenesis of osteomyelitis is multifactorial and poorly understood. Some important factors include: virulence of the infecting organism(s), underlying immune status of the host and the type, location and vascularity of the bone.
The suppurative infection is accompanied by oedema, vascular congestion and small?vessel thrombosis. The vascular supply to the bone is decreased by infection extending into the surrounding soft tissue in the early acute stage of the disease. When the medullary and periosteal blood supplies are compromised then sequestra may form. If treated quickly and insistently with antibiotics and, if necessary, with surgery, acute osteomyelitis can be halted prior to the development of dead bone. If there is an established infection, fibrous tissue and chronic inflammatory cells will form around the granulation tissue and dead bone. Early and specific treatment is important in osteomyelitis and identification of the causative microorganisms is essential for antibiotic therapy. The pathological features of chronic osteomyelitis are the presence of necrotic bone, formation of new bone and the oozing of polymorphonuclear leukocytes. New bone forms from the surviving fragments of periosteum and endosteum in the area of the
infection. An involucrum (an encasing sheath of live bone) encloses
the dead bone under the periosteum. The involucrum is irregular
and is usually perforated by openings; purulence may track into the
surrounding soft tissue and eventually drain to the skin surface,
forming a chronic sinus.
The major cause of bone infections is Staphylococcus aureus.
Infections with an open fracture or associated with joint prostheses
and trauma often require a combination of antimicrobial agents
and surgery. Biofilm?forming bacteria cause most infections; these
are a highly structured group of bacterial cells. Osteomyelitis can
also result from haematogenous spread after bacteraemia. When
prosthetic joints are associated with infection, microorganisms
typically grow in biofilm. The biofilm protects bacteria from antimicrobial
treatment as well as the host immune response.


Signs and symptoms
Haematogenous osteomyelitis is usually diagnosed clinically with
non?specific symptoms such as pyrexia, rigor, fatigue, lethargy or
irritability. The classic signs of inflammation, including local pain,
swelling, or redness, may also occur and generally disappear
within 5–7 days. There may be swelling and extreme tenderness
over the affected area, with associated erythema and warmth. As
the person moves, the pain is exacerbated and there may be sympathetic
effusion of neighbouring joints. Sometimes, the person
may present with mild symptoms, such as a history of blunt trauma
to the area, which may or may not be remembered, 24–48 hours
previously and mild or no pyrexia.
There may be chronic back pain with vertebral involvement
that is worse at rest and constant in nature. There may be a specific
complaint of pain at night. With contiguous osteomyelitis there is
also pain, pyrexia and erythema. However, the person may have an
associated history of accidental or surgical trauma
People with chronic osteomyelitis may have all or only a few of
the following: previous acute infection, localized bone pain, erythema
and swelling over the affected area, non?healing ulcers,
decreased range of motion of adjacent joints, chronic fatigue and
generalized malaise.


Investigations
A full blood count is performed (white cells are usually raised) and
inflammatory markers and blood cultures are required. Any
expressed pus needs to be cultured and also samples from joint
effusion taps and any potential primary sources (e.g. urine).
Bone cultures provide the gold standard for diagnosis. If a bone
biopsy is performed, it should be done through non?infected
tissue.
MRI is the imaging technique of choice. Plain X?ray films can
help in the diagnosis of chronic osteomyelitis


Management
Acute osteomyelitis can respond to antibiotic treatment alone.
Chronic osteomyelitis requires surgical debridement in addition to
antibiotic therapy. Analgesia (and limb splinting if a long bone is
involved) is a key aspect of symptom control. Treatment varies
according to the bones involved, severity of infection and immune
status of the patient.
Surgery may be needed to debride the bone and close any
defects.
In chronic osteomyelitis it is appropriate to delay treatment
until culture and sensitivity results are obtained, unless the infection
is severe, in which case empirical treatment is started as
above. Antibiotics are given for six weeks parentally. However, the
optimal duration of therapy for chronic osteomyelitis remains
uncertain
Surgical debridement is the mainstay of treatment (removing
necrotic tissue and providing an infection?free field for
future healing). Open?ended antimicrobial therapy may be
required if surgery is not possible; this is, however, less effective
than surgery.


Gout
Gout
This is an acute joint disease, an inflammatory arthropathy, an
arthritis, resulting in acute inflammatory state and subsequent tissue
damage. This is a very painful condition. It causes a spectrum
of disease.


Pathophysiology
Gout is a disorder of metabolism permitting uric acid or urate to
accumulate in blood and tissues; when supersaturated urate salts
precipitate forming needlelike crystals, these are less soluble under
acid conditions and at low temperatures, as occurring in cool,
peripheral joints of the metatarsophalangeal joint of the big toe.
Gout can be classified into primary or secondary gout subject
to the cause of hyperuricaemia. Primary gout occurs predominantly
in males aged 30–60 years who present with acute
attacks. Secondary gout is quite often due to chronic diuretic
therapy. It occurs in older people and is often associated with
osteoarthritis.
Gout affects the upper and lower limbs, with acute attacks. It
can present with painful, tophaceous deposits (there may be discharge)
in Heberden’s and Bouchard’s nodes.
The majority of people with hyperuricaemia never develop
gout and gouty patients may not have hyperuricaemia at presentation.
Most patients (about 90%) with gout develop excess urate as
a result of an inability to excrete adequate amounts of uric acid in
the urine. Most of the remaining patients either over consume
purines or produce excessive amounts of uric acid endogenously
(overproduction).
Most cases of primary gout are due to under?secretion of uric
acid. Fewer than 10% of cases are as a result of overproduction.
Many conditions and medications have been associated with an
increase in plasma urate levels, especially metabolic syndrome.
A genetic predisposition for hyperuricaemia exists; except in rare
genetic disorders, however, the development of gout in people who
are hyperuricaemic is mediated by environmental factors.
Overproduction of uric acid occurs in disorders that cause high
cell turnover, releasing purines present in high concentration in
cell nuclei. Cell lysis from chemotherapy can elevate uric acid levels,
as can excessive exercise and obesity. Causes of secondary gout
due to under excretion of uric acid include renal insufficiency,
starvation or dehydration, some drugs and chronic abuse of alcohol
(particularly beer and spirits).
The development of gout occurs where there are excessive stores
of uric acid in the form of monosodium urate. Uric acid is an endstage
by?product of purine metabolism, which is usually removed
by renal excretion. If excretion is ineffective in maintaining serum
urate levels below the saturation level of 6.8a•›mg/dL, hyperuricaemia
may develop. The presence of urate crystals in the soft tissues
and synovial tissues is a requirement for a gout attack. These
cA rystals can also be found in synovial fluid or on the cartilage
A surface in the absence of joint inflammation (see Figure 57.2).
A gout attack may be triggered by release of crystals (e.g. from
partial dissolution of a micro tophus caused by changing serum urate
levels) or precipitation of crystals in a supersaturated microenvironment.
In either situation urate crystals interact with intracellular and
surface receptors of local dendritic cells and macrophages, triggering
a danger signal activating the innate immune system, leading to
inflammatory mediator production.
There are several risk factors (comorbid conditions) associated
with a higher incidence of gout: hypertension, diabetes mellitus,
renal insufficiency, hypertriglyceridaemia, hypercholesterolaemia,
obesity, anaemia. Foods rich in purines: anchovies, sardines, sweetbreads,
kidney, liver and meat extracts, consumption of A?fructoserich
foods and beverages are associated with an increased risk of
gout. There is evidence that there may be a genetic link to gout.
The pathophysiology, clinical presentation and acute?phase
treatment of gout and pseudogout are similar; however, the underlying
causes of the diseases are very different. Many cases of
A?pseudogout in the elderly are idiopathic. Pseudogout has been
linked with trauma and a variety of metabolic abnormalities, for
example hyperparathyroidism and haemochromatosis.
Risk factors for pseudogout include use of loop diuretics and
proton pump inhibitors. Pseudogout has an underlying genetic
component, comorbid conditions (e.g. osteoarthritis) and environmental
factors may play a much stronger role.


Signs and symptoms
The development of acute pain in a joint that has become swollen,
tender and erythematous and which reaches its climax over a 6–12
hour period is highly suggestive of crystal arthropathy, though not
specifically of gout. Inflammation reaches its peak within 24 hours,
often with fever and malaise. Some people may only present with
connective tissue tophi.
There is evidence of synovitis and swelling and extreme tenderness
with overlying erythema. Atypical attacks can occur, with
tenosynovitis, bursitis and cellutitis lasting one or two days. There
may be irregular firm nodules mainly around extensor surfaces of
fingers, hands, forearms, elbows, Achilles tendons and ear, in
chronic tophaceous gout. Tophi are asymmetrical with a chalky
appearance under the skin.


Investigations
National guidelines are available that recommend investigations.
A clinical diagnosis can be made with reasonable accuracy with
typical presentations such as: inflammation of the first metatarsophalangeal
joint (known also as podagra) with hyperuricaemia;
presence of monosodium urate crystals in synovial fluid or tophi;
Gram staining and culture of synovial fluid. Serum uric acid levels
should be estimated but as a diagnostic tool this is limited. Renal
uric acid secretion (24?hour urine sample is needed) may be helpful
in diagnosis. Radiographs may be useful in chronic gout. CT scanning
can help in less accessible areas.


Management
Pain relief is a priority. The objective is to relieve pain and inflammation as quickly as possible. Rest and an ice pack may be useful; A elevate the joint and avoid trauma. Non?steroidal anti?A inflammatory drugs, colchicine and corticosteroids can help with pain and A inflammation. Lifestyle issues such as weight loss, exercise, diet, alcohol consumption and fluid intake should be discussed.