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1. Septic Arthritis
By
Dr.Syed Arsalan
Akbar
Resident Ortho CMH Peshawar

2. •Septicarthritisisinflammation of a synovial
membrane with purulent effusion into the joint
capsule, due to infection.
Synovial membrane
Membrane surrounding joint
cavity
Produce synovial fluid
Contain rich capillary networkfor
phagocytic and hyaluronate-
producing function

3. Causes of septic arthritis
Bacterial
•Non gonococcal
arthritis
•Gonococcal
arthritis
others
•Virus
•Fungi
•Mycobacteria etc.

4. Most common form of spread
Usually affect people with underlying medical problem
May result from penetrating trauma
Introduction of organisms during diagnostic and surgical
procedures. For eg arthroscopy and intra-articular injection
More common in children.
Osteomyelitis usually begin in the metaphyseal region,
from which it breaks through the periosteum into the
joint.

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

6. a) In the early stage, there is an acute synovitis with a purulent joint effusion
b) Soon the articular cartilage is attacked by bacterial and cellular enzyme.
c) If infection is not arrested , the cartilage may be completely destroyed
d) Healing then leads to ankylosis

7. ...
•Within 24-48 hrs of bacterial invasion:
•Infiltration by neutrophils
•Vascular congestion
•Synovial proliferation
•Within 1 week following bacterial invasion:
•Continual purulent effusion
•Continual synovial proliferation
•Infiltration by mononuclear cells
•Granulation tissue
•Abscess development
•Within 10 days after abscess formation:
•Cytokine induced protelytic enzymes are
released
•End result is joint destruction and or systemic
sepsis

8. If leftuntreated,it will spread to the underlying bone
and out of joint to form abscess and sinus.
Healingwith:
1.Complete resolution
2.Partial loss of articular cartilage and fibrosis of joint
3.Loss of articular cartilage and bony ankylosis
4.Bony destruction and permanent deformity

9. ACUTE BACTERIAL ARTHRITIS
•Staphylococcus Aureus – 50%
•Streptococcus species, such as Streptococcus
viridans, S Pneumoniae & group B streptocci
•Gram negative bacilli – 10% - E.coli & pseudomonas
– More common
•Sites : Monoarticular involvement - -85% , knee –
most common
•Other – hip , wrist, shoulder & ankle
•Sternoclavicular and sacroiliac joint -

10. PREDISPOSING FACTORS:
•Artificial joint implants
•Bacterial infection elsewhere in body
•Chronic illness or disease (such as diabetes,
rheumatoid arthritis, and sickle cell disease)
•Intravenous (IV) or injection drug use
•Medications that suppress immune system
•Recent joint trauma
•Recent joint arthroscopy or other surgery

11. In new born infants
 More on septicaemia
Rather than joint pain
 Baby is irritable &
refuse to feed
 Tachycardia withfever
 Joints are warmth,
tenderness, resistance
to movement
 Umbilical cord and
inflamed IV site should be
suspicious of source of
infection
Differ
I
a
n
cc
c
o
h
rd
il
i
d
n
r
g
e
to
n
age
oacute pain in single
large joint(esp hip)
oPseudoparesis
oChild is ill,rapid pulse
and swinging fever
oOverlying skin looks red
& superficial joint swelling
may be obvious
oLocal warmth and
marked tenderness
o All movements are
restricted by pain or spasm.
o Look for source of
infection from septic toe or
discharge ear
Inadults
 Often in the
superficial joint(knee,
wrist or ankle )
 Joints painful,
swollen & inflamed.
 Warmth and
marked local
tenderness &
movement restricted.
 look for gonococcal
infection or drug abuse.
 Patient with
rheumatoid arthritis and
especially those on
corticosteroid may
develop “silent” joint
infection.

12. Physical examination:
•Lower limb  antalgic limp / cannot walk
•Upper limb  affected part is closedly 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.

13. Investigations Explaination
Full blood count Elevated white blood cell count
ESR > 40 mm/hr
CRP > 20 mg/dL
Blood culture May be positive

14. Synovial fluid analysis
Aseptic technique is used during aspiration of synovial fluid.
Avoid taken from infected site ofskin.
The fluid is then analyzed by gross andmicroscopic
examination and culture.
Gross examinations include appearance, volume,
viscosity,
Microscopic examinations include leucocyte count,
staining of smears,, protein.
Finally, culture and sensitivity for definitive diagnosis
and treatment.

15. X ray
 Early Stage – Normal
Look for soft tissue swelling, loss of tissue planes,
widening of joint space and slight subluxation due to fluid in
joint. Gas may be seen with E. coli infection
 Late stage – Narrowing and irregularity of joint space
Plain film findings of superimposed osteomyelitis may
develop (periosteal reaction, bone destruction, sequestrum
formation).

16. Narrowing of joint space and irregularity of
subchondral bone.
Joint space loss
subchondral erosions and
sclerosis of the femoral
head
osteonecrosis and
complete collapse of
the femoral head

17. Ultrasonography-
•More reliable in revealing a joint effusion in
early cases.
•Widening of space between capsule and
bone of > 2mm indicates effusion.
•Echo-free  transient synovitis
•Positively echogenic  septic arthritis

18. CT scans, MRI, and bone
scans
•CT scans – soft tissue swelling, joint
effusions, abscess formation, guide joint
aspiration, monitor therapy and planning
operative approaches.
•MRI – extent of infection, diagnosing
infections that are difficult to access, better
anatomical detail.
•Bone scans- detect localized areasof
inflammation.

19. Treatment :
• The first priority is to aspirate the joint and examine the fluid,
treatment is then started without further delay.
• General measures:
- analgesics
- iv fluids
• Splintage-
-the joint must be rested either on a splint or in a widely split
plaster
-in neonates and infants, with hip infection the joint is held
abducted and 30 degree flexed, on traction to prevent
dislocation.
• Antibiotics –
- treatment is started once blood and samples are obtained.
-empirical treatment is started depending on most likelyorganism.

20.  Surgical Drainage
Indications:
-Joints that don’t respond to antimicrobial therapy and daily
arthrocentesis
-Any joint with limited accessibility, including the sternoclavicular or
the hip joint
-Patient with underlying disease( DM,RA, immunosuppression etc)
need more aggressive treatment with earlier surgical intervention
 Arthroscopic debridement and copious irrigation with
normal saline – more frequently in knee joint septic arthritis

21. -Bone destructionand dislocation of the
joint(esp Hip)
•Cartilage destruction
-may lead to either fibrosis or bony ankylosis
- in adult partial destruction of the joint will result in
secondary osteoarthritis
•Growth disturbance
- presenting as either localised deformity or shortening
of the bone

22. Gonococcal arthritis
- results from gonococcal infection (colonization of
urethra, cervix, pharynx)
-Sexually active healthy persons
-More common in women than men
-Congenital Complement deficiency

23. Clinical features-
•Disseminated gonococcal infection- fever,chills,
rash, small no. of papules that progresses to
haemorrhagic pustules present on trunk and
extensor surfaces of distal extremities.
•Migratory arthritis and tenosynovitis of the knees,
hand, wrists, feet and ankles.
•Cultures of synovial fluid are negative, blood
cultures positive < 45%, synovial fluid may be
difficult to obtain , usually contains 10000 – 20000
leucocuytes/micro L.

24. Treatment-
•Initiallly, ceftriaxone( 1 g IV every 24 h)
•Local and systemic signs resolve, oral antibiotic
(ciprofloxacin 500mg BD) should be started for 7
days.
•Penicillin susceptible- amoxiciilin 500 mg TDS .
•Suppurative arthritis usually respond to needle
aspiration and antibiotic treatment for 7-10 days.

25. Mycobacterial arthritis
• 1% of all cases of TB and 10% of extrapulmonary cases
• Pathology –
• Enters the body via lung(droplet infection) or the gut( swallowing
infected milk priducts), rarely through skin
• It causes granulomatous infection associated with tissue necrosis and
caseation.
• Primary complex – initial lesion in lungs , phayrnx or gut with
lymphatic spread to regional lymph nodes.
• Secondary spread- widespread dissemination via blood stream
giving rise to extrapulmonary lesions.
• Tertiary lesion- foci developing to destructive lesions.
• Once they get foothold they elicit a chronic inflammation.

26. synovium involved
becomes thick and oedematous, marked effusion
pannus of granulation tissue develops, articular cartilage
slowly destroyed, increased vascularity causes osteopenia
if unchecked, caseation and infection extend into surrounding
soft tissues and produce cold abscess
may burst forming sinus or tuberculous ulcer

27. Clinical features
•Previous history of infection or recent contact with
TB
•A long history of pain and swelling
•Marked synovial thickening
•Involvement of only one joint
•Severe muscle wasting
•Enlarged and matted regional lymph nodes
•Night cries, fever,night sweats, loss of weight.

28. treatment
•Rest
•Chemotherapy : two months course of
isoniazide(600mg), rifampicin(450mg),
pyrazinamide(1500mg), ethambutol(1200mg) thrice
weekly and then 4 months course of
isoniazide,ethambutol rifampicin thrice weekly.

29. Fungal arthritis
•Infection causes granulomatous reaction, often
leading to abscess formation, tissue destruction and
ulcer formation
•Superficial and deep infections.
•Superficial mycoses- primarily infections of skin and
mucous membrane. Eg, madurmycoses, sporothrix ,
candida, actinomycoses.
•Deep mycoses- blastomyces, histoplasma ,
Cryptococcus, coccidioides, aspergillus. Gain entry
through lungs.

30. Madurmycosis-
cut in foot
spread through subcutaneous tissues and along
the tendon sheaths
Bones and joints are infected by direct invasion,
local abscesses form and break through the skin as
multiple sinuses.

31. Clinical features
Subcutanoeus nodule, tender
Swollen foot, indurated
Discharging sinuses and ulcers
X- rays: multiple bone cavities , progressive bone
destruction
Organism can be identified in sinus discharge or
biopsy

32. treatment
•Intravenous amphotericin B advocated
•Necrotic tissue –excised
•Amputation- may be necessary

33. Viral arthritis
•Infects synovial tissue during systemic infections or
by provoking an immunologic reaction that involves
joints.
•Rubella- arthralgia , frank arthritis within 3 days of
rash following natural infection with rubella
•Parvovirus B 19- arthritis, arthropathy , stiffness of
joints
•Acute Hep B- arthralgia, fever, urticarial 2 weeks
before onset of jaundice.