INFECTIONS IN ORTHOPAEDICS

TOPICS

• Acute osteomyelitis • Septic arthritis

• Gonococcal arthritis
• Secondary osteomyelitis • Syphilis of joints
• Chronic osteomyelitis
• Fungal infections
• Garre’s osteomyelitis
• Leprosy and orthopaedics
• Brodie’sabscess
• Tuberculosis
• Salmonella osteomyelitis
ACUTE OSTEOMYELITIS

• Infection of the bone by micro-organisms is called Osteomyelitis.

• Osteomyelitis can be acute or chronic.
• Acute osteomyelitis can be primary (haematogenous) or secondary
(following an open fracture or bone operation)

AETIOPATHOGENESIS
Staphylococcus aureus is the commonest causative organism.
• Others are Streptococcus and Pneumococcus.
• These organisms reach the bone via the blood circulation
• The bacteria, as they pass through the bone, get lodged in the
metaphysis.
• The host bone initiates an inflammatory reaction in response to
the bacteria.
• This leads to bone destruction and production of an inflammatory
exudate and cells (pus).
• it spreads in the following directions.
-Along the medullary cavity: Pus trickles along the
medullary cavity and causes thrombosis of the venous and arterial
medullary vessels.
-Out of the cortex: Pus travels along Volkmann’s canals and
comes to lie sub-periosteally. The periosteum is thus lifted off the
underlying bone, resulting in damage to the periosteal blood supply
to that part of the bone. Eventually the periosteum is perforated,
letting the pus out into the muscle or subcutaneous plane, where it
can be felt as an abscess.
 -In other directions: The epiphyseal plate is resistant to the spread of
pus. At times it may be affected by the inflammatory process. The capsular
attachment at the epiphysis-metaphysis junction prevents the pus from entering
the nearby joint. In joints with an intra-articular metaphysis, pus can spread to
the joint, and cause acute pyogenic arthritis e.g., in the hip, in the shoulder etc.

DIAGNOSIS
The diagnosis of acute osteomyelitis is basically clinical.
Presenting complaints: The child presents with an acute onset of pain and
swelling at the end bone, associated with fever.
Investigations:
• Blood: There may be
polymorphonuclear leucocytosis
and an elevated ESR. .
• X-rays :The earliest sign
to appear on the X-ray is
a periosteal new bone deposition
•Bone scan: A bone scan using
Technetium-99 may show
increased uptake by the bone
in the metaphysis.
TREATMENT
Treatment depends upon the duration of illness after which the child is brought.
Cases can be divided into two groups:
a) If the child is brought within 48 hours of the onset of symptoms: it is
supposed that pus has not yet formed and the inflammatory process can be halted
by systemic antibiotics. Treatment consists of rest, antibiotics and general
building-up of the patient.
b) If the child is brought after 48 hours of the onset of symptoms: If the child is
brought late or if he does not respond to conservative treatment, it is taken for
granted that there is already a collection of pus within or outside the bone.
Surgical exploration and drainage is the mainstay of treatment. Rest, antibiotics
and hydration are continued post-operativelyent at this stage.
COMPLICATIONS
General complications: In the early stage, the child may develop septicaemia
and pyaemia.
Local complications:
1. Chronic osteomyelitis
2. Acute pyogenic arthritis
3. Pathological fracture
4. Growth plate disturbances
SECONDARY OSTEOMYELITIS

• This condition arises from a wound infection in open fractures or

after operations on the bone.
• The constitutional symptoms are less severe than those in
haematogenous osteomyelitis as the wound provides some
drainage.
• The condition can be largely prevented by adequate initial
treatment of open fractures, and adherence to sterile operating
conditions for routine orthopaedic operations.
CHRONIC OSTEOMYELITIS

• Conventionally, the term ‘chronic osteomyelitis’ is used for chronic pyogenic

osteomyelitis.
• The other causes of chronic osteomyelitis are tuberculosis, fungal infections
etc.
• three types of chronic osteomyelitis:
a) Chronic osteomyelitis secondary to acute osteomyelitis.
b) Garre’s osteomyelitis.
c) Brodie’s abscess.
• PATHOLOGY
Acute osteomyelitis commonly leads to chronic osteomyelitis
because of one or more of the following reasons:
a) Delayed and inadequate treatment : Delay causes spread of pus
within the medullary cavity and subperiosteally. This results in the
death of a part of the bone (sequestrum formation). Destruction of
cancellous bone leads to the formation of cavities within the bone.
Such ‘non-collapsing’ bone cavities and sequestra are responsible for
persistent infection.
B) Type and virulence of organism: Sometimes, despite early,
adequate treatment of acute osteomyelitis, the body’s defence
mechanism may not be able to control the damaging influence of a
highly virulent organism, and the infection persists.
• C) Reduced host resistance: Malnutrition compromises the body’s
defence mechanisms, thus letting the infection persist.
DIAGNOSIS
• Diagnosis is suspected clinically
• confirmed radiologically
• Presenting complaints: A chronic discharging sinus is the commonest
presenting symptom. Pain is usually minimal but may become aggravated
during acute exacerbations.
• Examination: •Chronic discharging sinus
. • Thickened, irregular bone
• Tenderness
• Adjacent joint
INVESTIGATIONS
*Radiological examination: The following are some of the salient radiological
features seen in chronic osteomyelitis:
• Thickening and irregularity of the cortices
• Patchy sclerosis
• Bone cavity: This is seen as an area of rarefaction surrounded by sclerosis
• Sequestrum
*Sinogram:
*CT scan and MRI
*Blood
*Pus: Pus culture may grow the causative organism.
TREATMENT

Principles of treatment: Treatment of chronic osteo-myelitis is primarily surgical

Operative procedures: Sequestrectomy.
Saucerisation.
Curettage.
Excision of an infected bone.
Amputation.
COMPLICATIONS
An acute exacerbation or ‘flare up’ of the infection ,Growth abnormalities,
pathological fracture , Joint stiffness ,Sinus tract malignancy.
GARRE’S OSTEOMYELITIS

• This is a sclerosing, non-suppurative chronic osteomyelitis.

• It may begin with acute local pain, pyrexia and swelling. Pyrexia and
pain subside but the fusiform osseous enlargement persists.
• There is tenderness on deep palpation.
• There is no discharging sinus.
• Shafts of the femur or tibia are the most commonly affected

Treatment :
• Acute symptoms subside with rest and broad-spectrum antibiotics.
• Sometimes, making a gutter or holes in the bone bring relief in pain.
 BRODIE’S ABSCESS

• It is a special type of osteomyelitis in which the body’s defense mechanisms have

been able to contain the infection so as to create a chronic bone abscess containing
pus or jelly-like granulation tissue surrounded by a zone of sclerosis.
• Common sites are the upper end of the tibia and lower-end of the femur.
• A deep boring pain is the predominant symptom.
• Radiological features: The radiological picture is diagnostic. It shows a circular or
oval lucent area surrounded by a zone of sclerosis.
• Treatment : Surgical evacuation and curettage is performed under antibiotic cover.
SEPTIC ARTHRITIS

• It is an arthritis caused by pyogenic organisms.

AETIOPATHOGENESIS: Staphylococcus aureus is the commonest causative
organism. Other organisms are Streptococcus Pneumococcus and Gonococcus.
DIAGNOSIS:
Presenting complaints:
• In its typical acute form, a child with septic arthritis presents with a severe
throbbing pain, swelling and redness of the affected joint. This is associated
with high grade fever and malaise.
INVESTIGATIONS
• Radiological Examination :
A careful look at the X-ray
may reveal
increased joint space and
a soft tissue shadow
• Blood shows
neutrophilic leucocytosis.
• Joint aspiration is the quickest and the best method of diagnosing septic
arthritis.
TREATMENT
In its early stage,
Diagnosis of septic arthritis must be confirmed or ruled out by joint aspiration.
Broad-spectrum antibiotics should be started by parenteral route.
In late cases,
After an arthrotomy and extensive debridement of the joint, it is immobilised in the
position of optimum function, so that as the disease heals, ankylosis occurs in that position.

COMPLICATIONS
1. Deformity and stiffness
2. Pathological dislocation
3. Osteoarthritis
GONOCOCCAL ARTHRITIS
• Gonorrhoea may be complicated by acute arthritis which arises within two
weeks of urethral discharge
• inflammation is confined to sub-synovial layer
• Often the inflammation subsides without pus formation.
• Onset is sudden, similar to septic arthritis, but the general condition of the
patient is well maintained in spite of severe local signs.
• Knee is the commonest joint affected.
• Penicillin is the drug of choice.
SYPHILIS OF THE JOINTS

• CONGENITAL SYPHILIS
The joint may be affected early or late in congenital syphilis.
Early: During infancy, osteochondritis in the juxta-epiphyseal region results in breakdown
of the bone and cartilage.
Late: A manifestation of congenital syphilis, ‘Clutton’s joints’ is a painless synovitis
occurring at puberty. It most commonly affects the knee and elbow, mostly bilaterally.
ACQUIRED SYPHILIS
The joints may be affected in the secondary and tertiary stages of acquired syphilis. In the
secondary stage, transient polyarthritis and polyarthralgia involving the larger joints
occur. In tertiary stage, gummatous arthritis occurs where the larger joints are most often
involved.
FUNGAL INFECTIONS

• Fungal infections of the bone occur usually in patients with suppressed

immunological status.
MADURA FOOT
• This is caused by Maduromycosis.
• It starts as a nodular swelling over the dorsum or sole of the foot.
• The nodule bursts and discharges a thin pus.
• Gradually more nodules form and result in a swollen foot with a nodular surface
and multiple discharging sinuses
• TREATMENT: In early stages, the lesion responds to massive doses of penicillin
or dapsone. In late cases, amputation may be necessary.
LEPROSY AND ORTHOPAEDICS

• Deformities are seen in all types of leprosy, but are more common in
tuberculoid and polyneuritic types.
• Mechanisms causing Disability: Nerve involvement leading to anaesthesia,
dryness of the skin, and paralysis, is primarily responsible for deformity and
disability of hands and feet.
• Clinical manifestations of leprosy are: (i) deformities; (ii) motor weakness
and muscle atrophy; (iii) trophic ulcers; (iv) mutilations; and (v) neuritis.
TUBERCULOSIS OF BONES AND JOINTS

AETIOPATHOGENESIS
• Common causative organism is Mycobacterium tuberculosis.
• Bone and joint tuberculosis is always secondary to some primary focus in the
lungs, lymph nodes etc.
•Mode of spread from the primary focus may be either haematogenous or by
direct extension from a neighbouring focus.
Pathology: Tubercular infection of the bone and synovial tissue produces
similar response as it produces in the lungs i.e., chronic granulomatous
inflammation with caseation necrosis
• The response may be proliferative, exudative or both;
• a) Proliferative response: This is the commoner of the two
responses. It is characterised by chronic granulomatous
inflammation with a lot of fibrosis.
• b) Exudative response: In some cases, particularly in immuno-
deficient individuals, elderly people and people suffering from
leukaemia etc., there is extensive caseation necrosis without much
cellular reaction. This results in extensive pus formation. These are
also termed non-reactive cases.
INVESTIGATIONS
• Radiological examination: X-ray examination of the affected part,
antero-posterior and lateral views, is the single most important
investigation.
• TB osteomyelitis: A tubercular osteomyelitis presents as a well-
defined area of bone destruction, typically with minimal reactive
new bone formation.
• TB arthritis: In tubercular arthritis there is reduction of the joint
space, erosion of the articular surfaces and marked peri-articular
rarefaction.
Other investigations:
• Blood examination: Lymphocytic leukocytosis, high ESR.
• Mantoux test: useful in children.
• Serum ELISA test for detecting anti-mycobacterium antibodies.
• Synovial fluid aspiration
• Aspiration of cold abscess and examination of pus for AFB.
• Histopathological examination of the granulation tissue obtained by biopsy
or curettage of a lesion.
Treatment
Principles of treatment: Treatment of tuberculosis of bones and joints consists
of control of the infection and care of the diseased part.
Control of infection: It is brought about by potent anti-tubercular drugs, rest
to the affected part and the building up of patient’s resistance.
Care of the affected part: This consists of protection of the affected part from
further damage, correction of any deformities and prevention of joint
contractures. Once the disease is brought under control, exercises to regain
functions of the joint are carried out.
Types :-

• TUBERCULOSIS OF THE SPINE-(Pott'sdisease)

• POTT’S PARAPLEGIA-(TB Spine with Neurological Involvement)
• TUBERCULOSIS OF THE HIP
• TUBERCULOSIS OF THE KNEE
• TUBERCULOSIS OF OTHER JOINTS-Other joints uncommonly affected
by tuberculosis are the elbow, shoulder and ankle joints
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