MUSCULOSKELETAL

INFECTION
NOR AIDA , JESSICA , NIVASINI , SARAH , SYARIFAH
OUTLINES
Osteomyelitis
Acute
Subacute
Chronic

Septic arthritis

Septic bursitis

Tuberculosis
OSTEOMYELITIS
INTRODUCTION
Osteomyelitis is inflammation of the bone caused by an infecting
micro-organism.
Although bone is normally resistant to bacteria colonization,
events such as trauma, surgery, presence of foreign bodies, or
placement of prostheses.
This may disrupt bony integrity and lead to onset of bone
infection.
Can progress into osteonecrosis, bone destruction and septic
arthritis and leads to permanent disability.
The major cause of bone infections is Staphylococcus aureus.
Classification:
ACUTE – within 2 weeks
SUBACUTE – 2 to 6 weeks
CHRONIC – After 6 weeks

Incidence of infection increases with increase in

grade of open fracture.
• Type I, II : 2%
• Type III : 10-50%
RISK FACTORS
Recent trauma
Immunocompromised recent
IV drugs use
Poor vascular supply
Systemic conditions. Eg: Diabetes, sickle cell disease
Peripheral neuropathy
ETIOLOGY
Age Group Most common organisms
Newborn (< 4 month) S. aureus, Enterobacter species, and group
A and B Streptococcus species
Children (4 months – 4 years) S. aureus, group A Streptococcus sp.,
Kingella kingae, and Enterobacter sp.
Children, adolescents (> 4 S. aureus (80%), group A Streptococcus
years to adult) sp., H. influenzae, and Enterobacter sp.
Adult S. aureus, and occasionally Enterobacter
or Streptococcus sp.
Sickle Cell Anemia Patients S. Aureus is typically most common, but
Salmonella sp. is Pathognomonic
PATHOPHYSIOLOGY
Bone normally resistant to infection.
When micro-organisms enter into bone hematogenously from
surrounding structures or from direct inoculation related to surgery
or trauma, osteomyelitis can occur.
Bone infection result from treatment, allows pathogen to enter bone
and proliferate in traumatized tissue.
When persists for months – chronic osteomyelitis.

Important factors in the pathogenesis:

• Virulence of infecting organism
• Underlying disease
• Immune status of the host
• Type, location and vascularity of the bone
Osteomyelitis can occurs in different ways. There are 3
mechanism of spread:

1. Hematogenous osteomyelitis
2. Coutiguous focus
3. Direct inoculation
• Penetrating injuries
• Surgical contamination
1. HEMATOGENOUS OSTEOMYELITIS
Adults, the vertebrae are the most common site of
hematogenous osteomyelitis, may also occur in the long
bones, pelvis, and clavicle.

Primary hematogenous: More common in infants and

children, usually occurring in the long bone metaphysis.
It may spread to the medullary canal or into the joint. When
infection extends into soft tissue, sinus tracts may
eventually form.

Secondary hematogenous: More common and occurs when

a childhood infection is reactivated. In adults, the location is
also usually metaphyseal.
S. aureus is the most common pathogenic organism recovered
from bone, followed by Pseudomonas and Enterobacteriaceae.
Less common organisms involved include anaerobe gram-
negative bacilli.
Intravenous drug users may acquire pseudomonal infections.
Gastrointestinal or genitourinary infections may lead to
osteomyelitis involving gram-negative organisms.
Dental extraction has been associated with viridans
streptococcal infections.
2. CONTIGUOUS-FOCUS AND POST-
TRAUMATIC OSTEOMYELITIS

The initiating factor in contiguous-focus consists of:

• Direct inoculation of bacteria via trauma
• Surgical reduction and internal fixation of fractures
• Prosthetic devices
• Spread from soft-tissue infection
• Spread from adjacent septic arthritis
• Nosocomial contamination

Infection usually results approximately one month

after inoculation.
Posttraumatic osteomyelitis: More commonly affects adults
and typically occurs in the tibia.

The most commonly isolated organism is S aureus. At the

same time, local soft-tissue vascularity may be compromised,
leading to interference with healing.

Compared with hematogenous infection, posttraumatic

infection begins outside the bony cortex and works its way in
toward the medullary canal.

Low-grade fever, drainage, and pain may be present.

Loss of bone stability, necrosis, and soft tissue damage may

lead to a greater risk of recurrence.
Minor trauma to the feet with multiple organisms isolated from
bone, including Streptococcus species, Enterococcus species,
coagulase-positive and -negative staphylococci, gram-negative
bacilli, and anaerobic organisms.

Foot ulcers allow bacteria to reach the bone.

• Patients may not experience any resulting pain, because of
peripheral neuropathy, and may present with a perforating foot
ulcer, cellulitis, or an ingrown toenail.
PAEDIATRIC OSTEOMYELITIS
Usually occurs after an episode of bacteremia in which the
organisms inoculate the bone.
The most common organisms isolated in these cases include S
aureus, Streptococcus pneumoniae, and Haemophilus
influenza type b (less common since the use of vaccine for H
influenza type b).
The incidence of Kinsella kingae infection is increasing; such
infection is a common cause of osteomyelitis in children
younger than 4 years.
The classical picture is seen in children between 2 and 6 years
old.
Usually starts in vascular metaphysis of a long bone – the
proximal tibia or in distal or proximal ends of femur.
OM in children can lead to pathologic fractures, about 5% of cases
with a 72-day mean time from disease onset to fracture.

Neonates: Hematogenous spread, especially in patients with

indwelling central venous catheters.
• The common organisms in osteomyelitis of the neonate include
those that frequently cause neonatal sepsis, namely group
B Streptococcus species, and E coli.
• Multiple osseous sites, and approximately half of the cases also
involve eventual development of septic arthritis in the adjacent joint.

Children with sickle cell disease

Increased risk for bacterial infections, and osteomyelitis is the
second most common infection in these patients.
The most common organisms involved in osteomyelitis in children
with sickle cell anemia include Salmonella species, S
aureus, Serratia species, and Proteus mirabilis.
ACUTE OSTEOMYELITIS
History Physical examination
Often diagnosed clinically with Scars or local disturbance of
nonspecific symptoms such as wound healing may be noted
fever, chills, fatigue, lethargy, or along with the cardinal signs
irritability. of inflammation.
The classic signs of Limited range of motion,
inflammation, including local deformity, and local signs of
pain, swelling, or redness, may impaired vascularity.
also occur and usually If periosteal tissues are
disappear within 5-7 days. involved, point tenderness
may be present.
COMPLICATIONS OF
ACUTE OSTEOMYELITIS
Most common complication in children with osteomyelitis is
recurrence of bone infection.
Common complications in children younger than 18 months:
• Bone destruction, chronic osteomyelitis, and impaired bone growth,
especially when the growth plate is affected.
Rarely, extreme bone destruction or thinning of the cortex can lead
to pathologic fractures.
Septic arthritis
Septicemia
Fracture
Overlying soft tissue cellulitis
Chronic osteomyelitis
INVESTIGATION
1. Blood
Leucocytosis
elevated ESR
Blood culture and sensitivity

2. Imaging
X ray
IMAGING
Radiographs performed early in the course of disease may
show subtle swelling of the deep soft tissue or edematous
subcutaneous soft tissues, but radiographs are often normal
in the first 7-10 days of infection.
By 10-14 days, a focal area of bone opacity develops in the
metaphysis.
This progresses to lytic destruction with an associated focal
periosteal reaction.
Radiographs typically show a well-
defined, longitudinally orientated,
ovoid lucency with surrounding
sclerotic margin but little or no
periosteal new-bone formation.
MANAGEMENT OF ACUTE OSTEOMYELITIS
 SUBACUTE OSTEOMYELITIS
Duration: 2-6 weeks.
Insidious in onset.
Caused by organisms of low virulence or a high resistance in
the host.

Main types: Brodie’s abscess

 BRODIE’S ABSCESS
Characterised by an abscess in the metaphyseal
area of long bone surrounded by a zone of sclerosis.

Caused by Staphylococcus.

Sites: Upper end of tibia / lower end of femur.

Clinical features:

 Adolescent patient.

 Intermittent attacks of deep-seated dull pain in

the region – worst at night, relieved by rest.

 P.E. : Tenderness and mild swelling.

Treatment: Antibiotics (6 weeks) or surgical

Xray: Circular or oral
evacuation and curettage of the cavity (if no
lucency surrounded by
response to treatment). zone of sclerosis
 CHRONIC
OSTEOMYELITIS
Duration: > 6weeks
Chronic infection of the bone involving osteoid
as well as myeloid tissues characterized by
presence of sequestra, involucrum and cloacae.
“A severe, persistent and incapacitating infection
of bone and bone marrow”

Common organism:
• Staph. Aureus (commonest)
Causes: • Staph. pyogenes
• Inadequately treated acute osteomyelitis. • E.coli
• Pseudomonas
• Weak host defense mechanism due to • Staph. epidermidis
malnutrition. (commonest in surgical
implant)
• High virulence of the organisms.
Pathophysiology:

In an attempt to
Migration of Lyses the bone
engulf the
leucocytes to the causing
Infection in bone infectious
infected area and decalcification of
organism, releases
hyperemia bone
enzymes

Necrotic
Impaired blood Dead cortex is
cancellous bone is
Pus spread into flow in bone and detached from
readily absorbed
bone blood vessel devitalized the living bone forming
and replaced by
infected bone sequestrum
new bone

Surrounding bone
Externally, the
attempts to wall of Involucrum has Extrusion of
periosteum lays
infection by small openings exudates, debris
down new bone
forming a thick, called cloacae and sequestra
called involucrum
dense wall
Clinical Features:
SYMPTOMS SIGNS
• Fever • Pus (seropurulent) discharging or healed sinus
• Pain and swelling during • Thickened, irregular and deformed bone
intermittent acute • Skin is dusky, thin, atrophic and poorly
exacerbations nourished
• Muscle and tissue scarring
• Joint contractures
Risk factors: • Pathological fractures (sometimes)
• Recent trauma or surgery • Deformity
• Immunocompromised • Limb length discrepancy (shortening or
patients lengthening)
• Illicit IV drug use • Restriction of joint movements due to
• Poor vascular supply extensive scarring
• Systemic conditions such
as diabetes and sickle cell
• Peripheral neuropathy
GARRE’S SCLEROSING OSTEOMYELITIS
Diffuse sclerosing inflammatory lesion.
Site: Shaft of long bones and mandible.
Clinical features:
Chronic pain in the leg with minimal or no
constitutional symptoms.
P.E. : Deep bone tenderness. No
discharging sinus.
Fusiform osseous enlargement persists.
Intense proliferation of periosteum
resulting in new bone deposition.
Differential diagnosis: Ewing’s sarcoma,
osteosarcoma, osteoid osteoma
Investigation:
1) Imaging – Aid in confirmation of diagnosis and to prepare for surgical treatment.

Plain radiographs
• Signs of cortical destruction
(corticomedullary moth eaten destruction).

• Periosteal reaction (involucrum).

• Sequestra (surrounded by a zone of
translucency-pus or granulation tissue).

• Cortical thickening and irregularities.

• Deformity.
• Pathological fracture (sometime).
Sinography CT
• If a sinus tract is present. • Provides excellent definition of
cortical bone.
• Valuable adjunct to surgical
planning. • Esp useful in identifying
sequestra.
• Methylene blue or radio-opaque
dyes to stain and differentiate
dead tissue from live during
Isotopic bone scanning
sinus excision.
• More useful in acute
osteomyelitis.
MRI
• Indium-111-labelled leucocyte
• Rim sign: Well-defined rim of scans are sensitive in
high signal intensity around the differentiating chronic
focus of active disease. osteomyelitis from neuropathic
arthropathy in diabetic foot than
• Sinus tracts and cellulitis:
technetium or gallium scans.
Increased intensity on T2–
weighted imaging. • Technetium-99m bone scans lack
specificity.
2) Laboratory analysis
3) Microbiology
Leukocyte count (WBC)
Blood cultures
• Often elevated in acute osteomyelitis • May be used to guide therapy
• May be normal in chronic for hematogenous osteomyelitis
osteomyelitis

Bone biopsy*
Erythrocyte Sedimentation Rate (ESR)
• Gold-standard for guiding
• Usually elevated in both acute and
antibiotic therapy
chronic osteomyelitis
• Decrease in ESR after treatment is a
favorable prognostic indicator

C-reactive protein
• Decreases faster than ESR in
successfully treated patients
CIERNY-MADER STAGING
(describes anatomic involvement, host, treatment, prognosis)

Medullary Osteomyelitis
Infection confined to
medullary cavity.
Superficial Osteomyelitis
Contiguous type of infection.
Confined to surface of bone.
Localized Osteomyelitis
Full-thickness cortical
sequestration which can
easily be removed surgically.
Diffuse Osteomyelitis
Loss of bone stability, even
after surgical debridement.
Treatment:
Drug therapy Surgical operations
Fusidic Acid, Clindamycin & Sequestrectomy
Cephalosporins Curettage
Vancomycin & Teicoplanin -MRSA) Sauceratization
Excision of sinus tract
IV route for 10-14days
Obliteration of dead space
Antibiotic is continued for another 6
Amputation
weeks (min) but usually > 3months.

When antibiotics can be stopped?

• Clinically: signs of healing, pain reduced/gone, no fever, can walk (LL OM),
no discharging sinus
• Inflammatory parameters (CRP, ESR) normalizes
• Serial x-ray : bone healing; no new OM changes
Complications:

• Acute-on-chronic osteomyelitis
• Stiffness of joints
• Pathological fractures
• Deformity Shortening - Destruction of
growth plate arrest growth.
• Limb length discrepancy
Lengthening - Stimulation of
• Malignancy growth plate due to hyperemia.
• Amyloidosis
SEPTIC ARTHRITIS
DEFINITION
Inflammation involving a joint from which
infecting micro-organism is either detected or
presumed to be the cause of infection.
PREDISPOSING FACTORS &
CAUSATIVE AGENTS
PREDISPOSING FACTOR CAUSATIVE AGENTS

• Rheumatoid arthritis • Usually Staph. Aureus

• Comorbidities • 1-4 years old:
• Intravenous drug Haemophilus
abuse Influenzae unless they
• Immunosuppressive have been vaccinated.
drug therapy/ • Occasionally other
immunosuppressive microbes have been
patients encountered.
- E.coli
- Proteus
- Neisseria gonorrhea (STD)
PATHOGENESIS Bacteria can gain entrance
into a joint by 3 routes:

Direct spread from

Haematogenous Direct inoculation
adjacent local infection

Most common form of Penetrating More common in children.

spread. Osteomyelitis usually begin
trauma/diagnostic &
in the metaphyseal region,
Usually affect people with surgical procedures.
from which it breaks
underlying medical Examples: arthroscopy & through the periosteum
problem. intra-articular injection into the joint.

Partly by the
As pus bacterial
Bacteria can Inflammatory
Synovial appear in enzyme, and
easily enter reaction with
membrane the joint, partly by the
synovial seropurulent
is highly exudate and
the articular enzyme
joint via released from
vascularised increase in cartilage is
blood synovium,
. synovial fluid eroded and
stream. inflammatory
destroyed.
cell and pus
 Adult
Infant Children
Effect confined on articular
Destroy the epiphysis, Vascular occlusion lead cartilage
which is still largely to necrosis of Extensive erosion can occur
cartilaginous. epiphyseal bone due to synovial proliferation
and ingrowth
 CLINICAL FEATURES
(DIFFERS ACCORDING TO AGE)

 More on septicaemia rather

than joint pain
 Baby is irritable & refuse to
feed
 Tachycardia with fever
NEW  Joints are warmth,
tenderness, resistance to
BORN movement
INFANTS  Umbilical cord & inflamed
IV site should be suspicious
of source of infection
 Check baby’s spine, chest
& abdomen to rule out
other sites of infection.
 o Acute pain in single large joint(esp hip/knee)
o Pseudoparalysis (reluctant to move limb)
o Ill, tachycardia & swinging fever
o Overlying skin looks red & superficial joint swelling
CHILDREN may be obvious .
o Local warmth & marked tenderness
o All movements are restricted by pain or spasm.
o Look for source of infection : septic toe or discharge
ear

 Often in the superficial joint(knee, wrist or ankle, toe

)
 Joints painful, swollen & inflamed.
 Warmth and marked local tenderness & movement
ADULTS restricted.
 Look for gonococcal infection or drug abuse.
 Patient with rheumatoid arthritis and especially those
on corticosteroid may develop “silent” joint infection.
 PHYSICAL EXAMINATION
Lower limb  antalgic limp / cannot walk
Upper limb  affected part is closely
guarded
Marked tenderness, active and passive
range of motion are limited
Examine for synovial effusion, erythema,
heat and tenderness.
Spasm of muscles around the joint may be
marked.
Patient may hold the joint in a position to
reduce the intra-articular pressure to
minimize pain.
 INVESTIGATIONS
Blood Imaging
• Full blood count: white cell count • Ultrasonography: most reliable method
increased for revealing joint effusion in early cases.
• CRP & ESR raised - widening of space between capsule &
CRP >20mg/dL bone >2mm = effusion
ESR >40mm/hr - echo-free (transcient synovitis)
• Blood culture: maybe positive - echogenic (septic arthritis)
• X-ray: soft-tissue swelling, loss of tissue
planes, widening of radiographic ‘joint
space’ & slight subluxation (fluid in joint).
- E.coli = sometimes gas in joints
- late: narrowing & irregularity of joint
• MRI & radionuclide imaging: obscure
sites (sarcoiliac & sternoclavicular joints)
 Narrowing of joint space and
irregularity of subchondral bone.

subchondral erosions and osteonecrosis and

Joint space loss sclerosis of the femoral complete collapse of
head the femoral head
 Synovial fluid analysis
• Aseptic technique is used during aspiration of
synovial fluid.
• Avoid taken from infected site of skin.
• Gross examinations: appearance, volume,
viscosity, mucin clotting (amount of
proteoglycans).
• Microscopic examinations : leucocyte count,
staining of smears, serum glucose ratio,
protein.
• Finally, culture and sensitivity for definitive
diagnosis and treatment.
 TREATMENT
First priority is to aspirate joint & examine fluid. Treatment is then started without further delay &
follow same lines for acute osteomyelitis

GENERAL SUPPORTIVE CARE SPLINTAGE(rest joint)

Analgesics = pain If hip infection, joint should be held abducted & 30
IV fluids = dehydration degrees flexed, on traction to prevent dislocation

ANTIBIOTICS (same guidelines as acute haematogenous OM)

Neonates & infants to 6 months: penicillinase-resistant penicillins (Flucloxacillin + 3rd gen
cephalosporin)
6 months – puberty: can be treated like above unless if not vaccinated, treat for
Haemophilus
Older teenagers & adults: flucloxacillin & fusidic acid. If initial exam shows Gram-negative
organism, 3rd generation cephalosporin is added.

Course: intravenously, 4-7 days → oral for another 3 weeks

 DRAINAGE
Under anesthesia, joint is opened through small incision, drained & washed out with
physiological saline.
A small cathether is left in place & wound is closed.
Suction-irrigation is continued for another 2-3 days.
Advisable for very young infants, if hip is involved and is aspirated pus is very thick.
Knee – arthroscopic debridement & copious irrigation may be equally effective.
Older children with early septic arhritis <3 days any joint except hip = repeated closed
aspiration.
- if no improvement within 48 hours = open drainage

AFTERCARE
Further damage is unlikely is patient’s general condition is satisfactory & joint no longer
painful/warm.
If articular cartilage has been preserved, gentle & gradually increasing active
movements are encouraged.
If articular cartilage has been destroyed = keep joint immobile while ankylosis is
awaited = splinting by plaster
 COMPLICATION
If left untreated, it will spread to Bone destruction and
the underlying bone and out of
dislocation of the joint (esp Hip)
joint to form abscess and sinus.

Cartilage destruction
• may lead to either fibrosis or bony ankylosis
Healing with: • in adult partial destruction of the joint will
• Complete resolution result in secondary osteoarthritis
• Partial loss of articular cartilage
& fibrosis of joint Growth disturbance
• Loss of articular cartilage &
• presenting as either localised deformity or
bony ankylosis shortening of the bone
• Bony destruction & permanent
deformity
SEPTIC BURSITIS
INFLAMMATION OF BURSAE DUE TO INFECTION
WHAT IS BURSAE?
ANATOMY
Bursae are flattened sacs that serves as protective buffers between
bones and overlapping muscles (deep bursae) or between bones and
tendons or skin (superficial bursae)

The synovial tissue lining the inner layer of bursae and produce fluid
inside the bursae to facilitate movement during muscle contraction.

Deep bursae (eg: subacromial and iliopsoas bursae) are located in

the fascia while superficial bursae (eg: olecranon and prepatellar
bursae) are located in the subcutaneous tissue.

There is 2 types of bursae: constant and adventitial.

 Constant Adventitial
• Form during embryonic • Form later in life in response
development to repeated trauma or
constant friction and pressure
• Lined with endothelial • Lack of endothelial cells
• Located between bones and • Do not contain synovial fluid
tendons or skin
• Contain synovial cells that • Examples include those that
secrete a lubricating fluid rich develop over a bunion and
in collagen and proteoglycans osteochondroma

Humans have approximately 160 bursae

Bursitis occurs when the synovial lining becomes thickened and

produces excessive fluid, leading to localized swelling and pain.
TYPE OF BURSITIS
Septic bursitis refers to inflammation of the bursa that is due to
infection, typically resulting from bacterial inoculation that is direct
(eg, puncture wound), spread from nearby soft tissues (eg,
cellulitis), or hematogenous (eg, bacterial endocarditis).
Nonseptic bursitis due to trauma, repetitive injury, crystal
diseases, and other systemic disorders
The following bursae are most commonly affected:

1. Subacromial
2. Olecranon
3. Trochanteric
4. Prepatella
5. Infrapatella

Symptom of bursitis may include the following:

1. Localized tenderness
2. Pain (aggravated by movement of the specific joint, tendon,
or both)
3. Edema
4. Erythema
5. Reduced movement
PATHOPHYSIOLOGY

When the synovial tissue that lining the bursa started to multiply, it
will become thickened (how? By changing the normal synovial tissue
to granulation tissue then followed by fibrous tissue) and at the same
time form more collagen and produce more fluid inside the bursal
sac.

This will lead to swelling of the bursae and produce pain.

However, in the septic bursitis condition, there is preceding trauma to

joint for example that allow the entrance of the bacteria and the
bacteria will inoculate inside the bursa and trigger the inflammation
process.
HOW WILL BE THE
PATIENT PRESENTED
TO HOSPITAL?
Localized tenderness

Decreased range of motion or pain with movement

Erythema or edema (seen in superficial bursitis)

History of repetitive movement (eg: frequent kneeling leading to

prepatellar or infrapatellar bursitis)

Tenderness at the site of the inflamed bursa.

If the bursa is superficial, physical examination findings are significant

for localized tenderness, warmth, edema, and erythema of the skin.

Reduced active range of movement with preserved passive range of

motion (this is not conclusive as tendinitis and musculoskeletal injury
also can presented the with reduce ROM)

In chronic bursitis, patient will try to avoid using the effected limb. So
can see atrophy and weakness of the limb. The tendon also may be
weakened and tender.
DIFFERENTIAL DIAGNOSIS
Septic arthritis
Ligamentous injury
Fracture
Osteoarthritis
Cellulitis
Gout and pseudogout
Rheumatoid arthritis
Soft tissue knee injury
WORKUP
1. Blood studies
2. Joint aspiration and fluid analysis
3. Plain radiography, Bone scanning, MRI and CT
4. Ultrasonography
Routine laboratory blood work is generally not helpful in the
diagnosis of noninfectious bursitis but is appropriate when septic
bursitis or underlying autoimmune disease is suspected.

Aspiration and analysis of bursal fluid should be done to rule out

infectious or rheumatic causes and may also be therapeutic

MRI is usually unnecessary but if needed is very sensitive for

identification of bursitis, can rule out suspected solid tumours
and define pathology for possible surgical excision.

The ultrasonography is useful for further imaging of the bursa

when the diagnosis is uncertain, and can guide diagnostic
aspiration or therapeutic injection.
TREATMENT AND MANAGEMENT

Conservative treatment to reduce inflammation is used for most

patients with bursitis and includes the following:
1. Rest
2. Cold and heat treatment
3. Elevation
4. NSAID
5. Bursal aspiration
6. Intrabursal steroid injections (with or without local anesthetic
agents)

Patient with suspected septic bursitis should be treated with

antibiotic while awaiting culture results.
Surgical excision of bursae may be required for chronic or
fequently recurrent bursitis. Surgery is reserved as a last resort
for patients in whom conservative treatment fails.

The operation is varies according to site.

Most patients respond well to conservative management. Patients

who do not respond to non-operative treatment or who have signs
of tendinous or ligamentous injury require further evaluation.
Consultation with a general or orthopedic surgeon or
rheumatologist may be helpful.
TUBERCULOSIS
PREDISPOSING CONDITIONS
• Chronic debilitating disorders
• Diabetes
• Drug abuse
• Prolonged corticosteroid medication
• AIDS
• Other disorders resulting in reduced defence mechanisms
SKELETAL MANIFESTATIONS
The skeletal manifestations of the disease are seen chiefly in
the spine and the large joints, but the infection may appear in
any bone or any synovial or bursal sheath.
PATHOLOGY
1. Mycobacterium tuberculosis (usually human, sometimes
bovine) enters the body via the lung (droplet infection) or
the gut (swallowing infected milk products) or, rarely,
through the skin.
2. In contrast to pyogenic infection, it causes a
granulomatous reaction which is associated with tissue
necrosis and caseation.
PRIMARY COMPLEX
The initial lesion in lung, pharynx or gut is a small one with
lymphatic spread to regional lymph nodes;
Usually the bacilli are fixed in the nodes and no clinical illness
results, but occasionally the response is excessive, with
enlargement of glands in the neck or abdomen.
Even though there is often no clinical illness, the initial infection
has two important sequels:
(1) within nodes which are apparently healed or even calcified,
bacilli may survive for many years, so that a reservoir exists
(2) the body has been sensitized to the toxin (a positive Heaf
test being an index of sensitization) and, should reinfection
occur, the response is quite different, the lesion being a
destructive one which spreads by contiguity.
SECONDARY SPREAD
If resistance to the original infection is low, widespread
dissemination via the blood stream may occur, giving rise to
miliary tuberculosis, meningitis or multiple tuberculous
lesions.
More often, blood spread occurs months or years later, perhaps
during a period of lowered immunity, and bacilli are deposited in
extrapulmonary tissues.
Some of these foci develop into destructive lesions to which the
term ‘tertiary’ may be applied.
TERTIARY LESION
The characteristic microscopic lesion is the tuberculous granuloma
(or ‘tubercle’)
– a collection of epithelioid and multinucleated giant cells surrounding
an area of necrosis, with round cells (mainly lymphocytes) around the
periphery.
Within the affected area, small patches of caseous necrosis appear.
These may coalesce into a larger yellowish mass, or the centre may
break down to form an abscess containing pus and fragments of
necrotic bone.
Bone lesions tend to spread quite rapidly.
Epiphyseal cartilage is no barrier to invasion and soon the infection
reaches the joint.
Only in the vertebral bodies, and more rarely in the greater
trochanter of the femur or the metatarsals and metacarpals, does
the infection persist as a pure chronic osteomyelitis.
If the synovium is involved, it becomes thick and oedematous, giving
rise to a marked effusion.
A pannus of granulation tissue may extend from the synovial
reflections across the joint; articular cartilage is slowly destroyed,
though the rapid and complete destruction elicited by pyogenic
organisms does not occur in the absence of secondary infection.
At the edges of the joint, along the synovial reflections, there may be
active bone erosion.
In addition, the increased vascularity causes local osteoporosis.
If unchecked, caseation and infection extend into the surrounding soft
tissues to produce a ‘cold’ abscess (‘cold’ only in comparison to a
pyogenic abscess).
This may burst through the skin, forming a sinus or tuberculous ulcer,
or it may track along the tissue planes to point at some distant site.
Secondary infection by pyogenic organisms is common.
If the disease is arrested at an early stage, healing may be by resolution
to apparent normality.
If articular cartilage has been severely damaged, healing is by
fibrosis and incomplete ankylosis, with progressive joint deformity.
Within the fibrocaseous mass, mycobacteria may remain
imprisoned, retaining the potential to flare up into active disease
many years later.
 CLINICAL FEATURES
1. History of previous infection
2. Recent contact with TB
3. Pain and swelling
4. Fever, night sweats, lassitude and loss
of weight
5. ‘Night cries’; the joint, splinted by
muscle spasm during the waking hours,
relaxes with sleep and the inflamed or
damaged tissues are stretched or
compressed, causing sudden episodes
of intense pain.
6. Muscle wasting
7. Synovial thickening
8. Enlarged and tender regional lymph
nodes
9. Limited ROM in all directions
10. Joint stiffness and deformity
11. In tuberculosis of the spine, pain may be deceptively slight –
often no more than an ache when the spine is jarred.

12. Consequently the patient may not present until there is a

visible abscess (usually in the groin or the lumbar region to one
side of the midline) or until collapse causes a localized kyphosis.

13. Occasionally the presenting feature is weakness or instability

in the lower limbs.
 X-RAY

1. Soft tissue swelling

2. Peri-articular osteoporosis
3. Bone ends – ‘washed out’ appearance
4. Narrowed articular space
5. In children, the epiphyses may be
enlarged ; result of hyperaemia
6. Subcorticular bone erosion;
inflammatory process in the synovium
7. Cystic lesions
8. Spine; bone erosion and collapse
around a diminished intervertebral
disc space; the soft-tissue shadows
may define a paravertebral abscess
 OTHER INVESTIGATIONS
1. ESR - usually increased and there may be a relative lymphocytosis.
2. The Mantoux or Heaf test will be positive
i.e. a negative Mantoux virtually excludes the diagnosis, but a positive test
merely indicates tuberculous infection, now or at some time in the past.
3. Synovial fluid aspiration:
- Cloudy
- the protein concentration is increased
- the white cell count is elevated
- Acid-fast bacilli are identified in synovial fluid in 10–20 per cent of
cases, and cultures are positive in over half.
4. A synovial biopsy sections will show the characteristic histological
features and acid-fast bacilli may be identified;
 DIAGNOSIS
1. Transient synovitis
- Fairly common in children
- Always settles down after a few weeks rest in bed
- If synovitis recurs, further investigation ( even a biopsy) may be necessary
2. Monoarticular rheumatoid arthritis
- Starts in a single large joint
- Clinically distinguishable from TB
- Based on the results of synovial biopsy
3. Subacute arthritis
4. Haemorrhagic arthritis
- If the bleeding has followed a single recent injury, the history and absence
of marked wasting are diagnostic.
- History of bleeding elsewhere
5. Pyogenic arthritis
- Exclude an old septic arthritis
TREATMENT
1. REST
- This often involved splintage of the joint and traction to overcome
muscle spasm and prevent collapse of the articular surfaces.

- With modern chemotherapy this is no longer mandatory; rest and

splintage are varied according to the needs of the individual patient.

- Those who are diagnosed and treated early are kept in bed only until
pain and systemic symptoms subside, and thereafter are allowed
restricted activity until the joint changes resolve (usually 6 months to
a year).

- Those with progressive joint destruction may need a longer period of

rest and splintage to prevent ankylosis in a bad position; however, as
soon as symptoms permit, movements are again encouraged.
2. CHEMOTHERAPY
A combination of antituberculous drugs
The following is one of several recommended regimens

1. ‘intensive phase treatment’: bactericidal attack

isoniazid 300–400 mg, rifampicin 450–600 mg and fluoroquinolones 400–600
mg daily for 5 or 6 months.

2. ‘continuation phase treatment’: is to eliminate the ‘persisters’,

slow-growing, intermittently-growing, dormant or intracellular
mycobacteria.
isoniazid and pyrazinamide 1500mg per day for 4½ months and isoniazid
and rifampicin for another 4½ months.

3. ‘prophylactic phase’:
isoniazid and ethambutol 1200 mg per day for a further 3 or 4 months.
3. OPERATION
 Operative drainage or clearance of a tuberculous focus is
seldom necessary nowadays.
 However, a cold abscess may need immediate aspiration or
draining.
 Once the condition is controlled and arthritis has completely
subsided, normal activity can be resumed, though the patient
must report any renewed symptoms.
 If, however, the joint is painful and the articular surface is
destroyed, arthrodesis or replacement arthroplasty may be
considered.
 The longer the period of quiescence, the less the risk of
reactivation of the disease; there is always some risk and it is
essential to give chemotherapy for 3 months before and after
the operation.
REFERENCES
Apley's and Solomans Consise System of Orthopedics and Trauma 4th% Ed.
Medscape
Orthobullets