dr ikenna arthropods septic arthritis.ppt

topic is on septic arthritis and management

1. Seminar presentation

2. Outline
i

3. introduction
•Septic arthritis represents a true orthopaedic
emergency characterized by the invasion of
pathogenic micro-organisms into the joint
space ,resulting in purulent synovial
inflammation with devastating consequences
In pediatric patients with sickle cell disease ,
the condition takes on added complexity due
to underlying hematological abnormalities and
immuno-compromised status .

4. introduction
•Sickle cell disease affects the hemoglobin structure it is a
point mutation where HbS arises from a mutation
substituting thymine for adenine in the sixth codon of the
beta-chain gene, GAG to GTG. This causes coding of valine
instead of glutamate in position 6 of the Hb beta chain
leading to the production of abnormal hemoglobin s which
results polymerizes and becomes sickled when oxygen levels
drop . This damages blood vessel linings and boost
inflammation , making it easier for bacteria to stick and
invade . These patients aalso have increased susceptibility to
infection due to functional asplenia and impaired immunity

6. Relevant anatomy
•The knee is a synovial joint formed by
the fermur , tibia and patella ,
stabilized by ligaments (ACL,
PCL,MCL,LCL)
•Synovial membrane lines the joint
capsule , producing synovial fluid for
lubrication and nutrition .
•The vascular anatomy of the
paediatric knee , is particularly
relevant in septic arthritis as the
metaphyseal arteries form slow –
flowing loops near the growth plate ,
creating an environment where blood
–borne pathogens readily extravasate
into the joint space .

8. Epidemiology
•Septic arthritis affects about 5-12 out of every 100000 children
each year , with highest rates in kids under 3 . In SCD , the lifetime
risk jumps to 0.2-5.4%, especially in those with the severe SS type ,
due to immune vulnerabilities .
•World wide , SCD impacts around 300000n newborns annually ,
with the highest burden in sub-saharan Africa (1-2% of births). The
knee is involved in 20-30% of paediatric cases right after the hip .
•In the USA rates in SCD have dropped due to preventive penicillin
and vaccines but in low-resource areas , upto 10% of SCD children
get it . Boys are affected twice as often as girls . And in SCD
Salmonella bacteria cause infectiuons 2-3 times more frequently
than usual staphyloccoccus aureus in healthy kids .

9. Etiology
Most common cause in kids at all ages include
staphylococcus aureus(40-50% of cases ) ,
strepococcus species(20%) and kingella kingae . But
in SCD , salmonella species dominate (upto 70% in
some studies ) because gut bacteria can leak into
the blood during crises particularly with bowel
infarction and the immune system cant clear them
due to functional asplenia . Other culprits inlcude
gram-negative organisms like E.coli in newborns or
anaerobes after injuries

11. Pathophysiology
•Bacteria get seeded into the joint space via the heamatogenous
routes especially in SCD patient , direct innoculation from
trauma and contiguous spread from osteomyelitis .
•The inflammatory cascade triggered by joint infection follows a
characteristic sequence. Bacteria within the joint space release
exo-toxins and cell wall components that activate Toll-like
receptors on synovial cells, triggering the release of pro-
inflammatory cytokines including TNF-α, IL-1β, and IL-6. This
cytokine storm recruits neutrophils to the joint, where they
release proteolytic enzymes (matrix metalloproteinases,
elastase, cathepsins) and generate reactive oxygen species that
collectively degrade cartilage matrix components

13. Pathophysiology
• Also The resulting accumulation of purulent material within the
confined joint space leads to elevated intra-articular pressure,
potentially exceeding perfusion pressure and causing avascular
necrosis of articular structures .
In SCD patients, this destructive process is amplified by pre-
existing pro-inflammatory states characterized by chronic
elevation of acute-phase reactants and immune activation.
Additionally, functional defects in the alternative complement
pathway and impaired opsonization further compromise bacterial
clearance, allowing for unchecked microbial proliferation and
more rapid joint destruction compared to non-SCD patients
 

17. Classification
•Based on aetiology : bacterial (most common ) fungal ,viral.
•By joint involvement :monoarticular (knee common),
polyarticular(rare in children)
•By time duration : acute (symptoms <2 weeks ) , subacute
(2weeks – 3 months ) and chronic forms (> 3 months )
•Gachter classification (arthroscopic )
–Stage 1 opalescent fluid , synovial hyperemia
–Stage II : purulent fluid , fibrin deposits .
–Stage III : synovial thickening compartment formation
–Stage IV : Aggressive pannus , cartilage /bone erosion

18. Clinical presentation
•History :the child will usually present with complaints of
inability/refusal to move affected legs , with pain at the
affected joint ,there could be fever , swelling of the joint . With
a background history of injury to the leg secondary to a fall ,
prior illness or a patient with sickle cell disease which could be
mistaken for vaso-occlusive crisis.
•Physical examination : typically reveals a toxic –appearing child
with high fevers and signs of sepsis (tachycardia, tacypnea,
poor perfusion ) especially in advanced cases . In SCD, patients
usually appear pale , malnourished , with guarding and limited
range of motion of affected knee classic signs include

19. Clinical presentation
•Swelling and effusion , heat and erythema , tenderness ,
positional preference ( the knee is typically held in a position
of maximum comfort usually slight flexion (30 – 45 degrees)
•In children with sickle cell , the examination should include
careful assessment for abdominal tenderness (suggesting
salmonella gastroentritis and signs of acute chest syndrome
or other related sickle cell complications that might co-exist
with joint infection.
•A thorough musculoskeletal examination should also assess
for other joints, neurovascular status and signs of concomitant
osteomyelitis such as tenderness away from joint line

20. Differential diagnosis
•Vaso-occlusive painful crisis
•Osteomyelitis
•Transient synovitis
•Acute rheumatic fever
•Juvenile idiopathic arthritis
•Gout and pseudogout
•Traumatic hemarthrosis
•Avascular necrosis

21. Investigations
•Fbc (wbc > 12000mm3 with leukocytosis, hb is
reduced )
•ESR (40mm/hr) lacks specificity
•CRP (20mg/l)
•Seucr
•Viral screening ( RVS , Hbsag, HCV etc )
•Arthrocentesis and synovial fluid analysis ( represents
the gold standard for diagnosis and should be done
urgently )
–Synovial fluid findings diagnostic for septic arthritis include

22. Investigations
–Gross appearance –turbid or pururlent fluid
–White blood cell count :typically > 50000 cells
–Neutrophil predominance > 75 -90 %
polymorphonuclear cells
–Gram stains: posistive in 50-70% of cases
–Culture positive in 70 -90 % of cases if obtained prior to
antibiotics
–Glucose : reduced compared to serum level (< 40mg/dl )
–Lactate : elevated levels (>5 mmol/l) suggest bacterial
infection

23. Imaging
•Radiograph:should be obtained initially to evaluate for
alternative diagnoses such as fracture, malignancy, or
osteomyelitis. Early in septic arthritis, radiographs may show
only soft tissue swelling, joint space widening, and
displacement of fat pads. Later findings include joint space
narrowing (indicating cartilage destruction), periarticular
osteopenia, and erosive changes.
Ultrasound: is exceptionally valuable for detecting joint
effusion, guiding arthrocentesis, and assessing for extra-
articular complications. Its sensitivity for detecting effusions
approaches 95%, and it can identify complexities within the
fluid such as septations or debris that may suggest infection

24. Imaging
•.
MRI . Characteristic findings include synovial enhancement, bone
marrow edema, periarticular soft tissue inflammation, and
abscess formation. MRI is particularly useful in SCD patients for
distinguishing between bone infarction and infection, though
both may coexist .
Nuclear medicine studies (three-phase bone scan) have
traditionally been used to distinguish osteomyelitis from
infarction but have largely been replaced by MRI in centers where
it is readily available. The bone scan typically shows increased
uptake in all three phases (blood flow, blood pool, and delayed) in
both osteomyelitis and septic arthritis, limiting its specificity.

27. management
•management of paediatric SCD patient s with
septic arthritis is a multidisciplinary approach
involving the paediatric orthopaedic surgeon,
hematologist , paediatrician , infectious disease
specialist .
•the aim of management is to
•clear the infection
•stop further joint damage and rehabilitate
patient .

28. management
•empirical antibiotics should be started initially
after arthrocentesis, and later adjusted for the
organism culture.
•Empiric Coverage for SCD Patient:
• · Cover for Staph (including MRSA) and
Salmonella:
• · Vancomycin + 3rd Generation
Cephalosporin (Ceftriaxone/Cefotaxime)

29. management
•Adjunctive therapies are particularly important in SCD patients:
•· Pain management: Multimodal approach including opioids,
NSAIDs,
•· Hydration: Aggressive IV hydration to maintain adequate
perfusion and prevent sickling
•· Transfusion therapy: Consideration for packed red blood cell
transfusion to maintain Hb >10 g/dL and HbS <30% to improve
oxygen delivery and reduce sickling
•· Fever control: Acetaminophen and cooling measures to reduce
metabolic demand
•· Nutritional support: High-calorie, high-protein diet to support
immune function and healing

30. management
•surgical irrigation and debridement is mandatory.
•·Should be done within 24 hours of presentation, sooner
if possible.
•· Options:
• · Arthrotomy (Gold Standard): Open surgical drainage,
irrigation, and debridement. Allows complete
visualization of the joint.
• · Arthroscopy: Increasingly popular. Less invasive, allows
irrigation and debridement. Excellent for the knee joint.
•· Post-Op: Joint is often left open or closed over a drain.

31. Complications
• Osteomyelitis: Occurs in
 
60-70% of SCD patients with septic
arthritis due to direct extension or hematogenous spread
• Sepsis and multiorgan failure: Particularly concerning in
functionally hyposplenic SCD patients
•Avascular necrosis: Elevated intra-articular pressure can
compromise blood supply to epiphyses
•Pathological dislocation: From capsular destruction and
ligamentous laxity
• Growth disturbance: From damage to physes, leading to
limb length discrepancy

32. Complications and prognosis
•
Long-term sequelae occur in approximately
 
25-50% of cases despite appropriate treatment:
• Joint contractures: From capsular fibrosis and
muscle atrophy
• Cartilage loss and premature osteoarthritis:
Due to enzymatic destruction of articular
cartilage

33. Complications and prognosis
• Chronic pain: From articular damage and secondary
degenerative changes
•Functional impairment: Limiting mobility and participation in
activitie
• Recurrent infection: Particularly in patients with retained
necrotic debris or sinus formation
Prognostic factors associated with poor outcomes include:
· Delay in diagnosis >4-5 
days
· Infection with MRSA or Gram-negative organisms
· Concomitant osteomyelitis
· Young age (<2 years) at time of infection
· Multiple joint involvement
· Significant radiographic changes at presentation

34. Rehabilitation
•Immobilization: Initially, splint for comfort.
•· Early Mobilization: As pain allows, begin
gentle passive and active-assisted range of
motion to prevent stiffness and contracture.
•· Physical Therapy: Crucial for regaining
strength and function.
•· Monitoring:
• · Clinical exam (pain, swelling, ROM).

35. Follow up and prevention
Preventive strategies for septic arthritis in children with SCD focus on
reducing bacteremia risk and enhancing immune function:
1. Penicillin prophylaxis from 2 months to at least 5 years of age (or until
splenectomy) to prevent encapsulated organisms
2.Vaccination against Streptococcus pneumoniae, Haemophilus influenzae
type b, and Neisseria meningitidis per SCD-specific guidelines
3.Annual influenza vaccination to reduce risk of secondary bacterial infections
4.Prompt management of febrile illnesses with early evaluation and empirical
antibiotics when indicated
5. Family education about signs of joint infection and need for urgent
evaluation
6.Hydroxy urea therapy to reduce crisis

36. Follow up and prevention
•
Long-term follow-up is essential for early detection of
complications and functional impairment. Patient
should have a scheduled visit plan
Each visit should include assessment of growth, limb
length and symmetry, joint function, and radiographic
evaluation when indicated. MRI should be obtained in
patients with significant joint damage to monitor for
avascular necrosis and early degenerative changes .

37. Loco-regional challenges

38. Future trends in management

39. conclusion
•Treating knee septic arthritis in a young SCD
child demands a team effort from fast
diagnosis and custom antibiotics to surgery
when needed to counter the extra dangers
from the disease's biology. Acting early saves
the joint, and new techology will make
outcomes even better for these at-risk kids.

40. •THANK YOU .