ORTHOPEDIC INFECTIONS

Peads Team
SOFT TISSUE INFECTIONS
 Classifications
Soft Tissue
Infection

Complicated STI
Simple STI

1. Furuncles
2. Carbuncles
Diabetic Foot Necrotizing STI
3. Abscesses
4. Erysipelas
5. Cellulitis

Necrotizing Gas Forming

fascitis Myonecrosis

Lecture Bone and Soft Tissue Infections, Year 2 Musculoskeletal Block, Ass. Prof. Dr. Siti Suraiya
Md Noor
 cSTI Definition

Abscess Cellulitis Ulcer

Skin/skin
Skin/skin structure
structure infections
infections that:
that:
•• Involve
Involve deep,
deep, soft
soft tissue
tissue
•• Require
Require surgical
surgical intervention
intervention
•• Require
Require antimicrobial
antimicrobial therapy
therapy
•• Are
Are associated
associated with
with significant
significant underlying
underlying disease
disease
that
that complicate
complicate the
the response
response toto treatment
treatment
Lecture Bone and Soft Tissue Infections, Year 2 Musculoskeletal Block, Ass. Prof. Dr. Siti Suraiya
Md Noor
Anatomy of the skin

Microbiology Big Picture, Chapter 3, pg 39

 Gas Gangrene
1. Definition
2. Etiology
3. Risk Factors
4. Pathogenesis
5. Clinical Features
6. Complications
7. Investigations
8. Treatment
 Definition
GAS GANGRENE
Gas producing organisms like Localized cell death by
Clostridium obstructed circulation with
perfringens(welchii) superadded bacterial infection.

Gangrene complicated with bacterial infection by

gas producing organisms leading to gas
accumulation within the gangrene
 Etiology
1. Genus Clostridium
- Clostridium perfringens **
- C. ramosum
- C. bifermentans
- C. histolyticum
- C. novyi

2. Aerobic gram-negative bacteria

– Escherichia coli
– Proteus species
– Pseudomonas aeruginosa
– Klebsiella pneumoniae
83.3% of aerobic gram-negative bacilli
4.5% anaerobic gram-positive bacilli- Clostridium sp
http://emedicine.medscape.com/article/217943-overview#a5
 Clostridium perfringens

Spores are rarely seen in culture media or

material from pathogenic lesions, however
if present it is a characteristic morphologic
feature

Blood agar: Large, smooth, low convex, Gram stain: Gram positive bacilli with
circular, translucent colonies with a double sub terminal spore
zone of hemolysis; a complete zone of
hemolysis (B haemolysis) and a wider zone
of incomplete hemolysis (a-haemolysis)
Robertson Cooked Meat Media - meat to turn pink with sour smell and acid reaction.
 NAGLER REACTION

Observance Inference
A zone of opacity in the antitoxin-free half
Modified Eggonly but
Yolk not is
Agar onaother half due
differential andtoenriched medium  Lecithinase positive
used in the isolation and
presumptive nuetralization
differentiationof of
thedifferent
alpha toxin.
species based on their lecithinase and lipase
production Aand proteolytic
zone of opacityactivity.
on both The degradation
sides of lecithin present in the egg yolk results
of the plate
in the formation
or no of the agar. around the colonies. Lecithinase
opaqueonprecipitate
reaction The Lipasenegative
enzyme hydrolyzes the
fats within the egg yolk, which results in an iridescent sheen on the colony surface. 
 Source of Infection
• Contaminated, manured or cultivated soil
• Faecal flora and resident of mammals
intestines

08-02-2016
GAS GANGRENE BY DR.R.DURAI MGMCRI 12
 Risk factors
Post-traumatic Post-operative Spontaneous

• car • Clostridial • Usually occur

accidents (most infection in patient who
common) following case have severe
• crush injuries
of colon underlying
• gunshot wounds resection condition.
with foreign • Rupture Example :
bodies
• burns and appendix • colorectal ca
frostbite • Bowel • hematological
• IV drug abuse perforation malignancy
• Farm/industrial • Diabetes
injuries
contaminated
with soil

Any situation that leads to an anaerobic environment

- Dirty wound with dead muscle that has been closed without adequate debridement
 Injury Aerobic metabolism Co2 + H2O.
Anaerobic metabol.  H, N, H2S.

Anaerobic environment created (Low

partial pressue of oxygen)

Exogenous infection with

Clostridium perfringes

Bacterial toxins
- A - toxin

Facultative anaerobes (E.coli) start to switch to

Destroy WBCs, occlude arterioles and anaerobic respiration
veins

Insoluble gases form under the skin

Ischemia, edema, inflammation Gas accumulation

GAS GANGRENE
Gangrene
(Oedema, Necrosis, Toxaemia, Myositis)
 Clinical Features
• Pain - sudden and gradually worsen within 24 hours of injury
• Low grade fever
• Local swelling and massive edema over the affected area
• Skin changes - Bronze colour  blue black colour with skin blebs
and hemorrhagic bullae, within few hours, entire region become
edematous
• Characteristic smell
• Gas production (not very marked) - crepitus within the soft tissues
• Tachycardia
• Late signs  low BP, renal failure and altered mental status
 Investigations

• FBC – LDH increase, WBC low * and Hb level

low (hemolytic anemia)
• Blood C&S to determine the bacteria causing
the infection
• Swab C&S and Gram stain
• X ray – gases in the soft tissue, TRO OM
changes
 Gas Gangrene
• Treatment
RESUSCITATION!!
1) Antibiotic – Benzylpenicillin + Metronidazole +-
Gentamycin
2) Hyperbaric oxygen therapy
3) Surgical debridement – to remove all necrotic tissue
until the wound has clean and healthy granulation
tissue
4) Amputation of extremity is considered for life saving
 Hyperbaric oxygen therapy
• 2 main functions:
– To increase PO2 for a good tissue perfusion and in
turn promoting wound healing
– Suitable to use in any infective case suspecting of
anaerobes infection
 Complications
Patients with gas gangrene frequently develop:
• Massive hemolysis
• Shock
• Renal failure
Necrotizing
fasciitis
 Necrotizing Fasciitis
A progressive life-threatening soft-
tissue infection (with liquifactive
necrosis of subcutaneous fat and
fascia) ± skin .
Cheng NC, Su YM, Kuo YS, Tai HC, Tang YB. Factors affecting the mortality of necrotizing fasciitis
involving the upper extremities. Surg Today. 2008;38(12):1108-13
 Necrotizing Fasciitis
• Causative agents – bacteria, may be aerobic or
anaerobic or mixed flora
• Type 1 – polymicrobial flora (arise following
abdominal surgery or in DM)
• Type 2 – monomicrobial - group A strep.
(spontaneously in healthy pt.) [Strep.
pyogenes]
 Necrotizing Fasciitis
**Cofactors that Increase risks
• Diabetes
• Alcoholism
• Immuno-suppression
• Severe illnesses: heart, lung or liver disease
• Hx of recent trauma / Surgery
 Diagnosis

It is mainly a Clinical Diagnosis.

LAB: LRINEC
Lab Risk Indicator for NECrotizing fascii.
PARAMETER POINTS
CRP > 150 mg/L 4

Leucocytosis 15 – 25 X 103 1
> 25 X 103 2
Hb 11 – 13 g% 1
< 11 g% 2
Serum Na < 135 Meq / L 2

Serum Glucose > 180 mg % 1

> 6 should raise suspicion of NF

> 8 is highly predictive of NF
• Biopsy
A)  indications
– emergent frozen section can confirm diagnosis in early cases 
B) technique
– take 1x1x1cm tissue sample
– can be performed at bedside or in operating room
– surgical intervention should not be delayed to obtain
C) histological findings
– necrosis of fascial layer
– microorganisms within fascial layer
– PMN infiltration
– fibrinous thrombi in arteries and veins and necrosis of arterial and
venous walls
 Necrotizing Fasciitis
Investigations
• FBC- very highly-elevated WBC
• Ultrasound-reveal subcutaneous emphysema
spread along deep fascia, swelling and increase
echogenecity
• Aspiration and gram stain- to indentify causative
organism
PLAIN X RAY of an established
case of necrotizing fasciitis of
lower limb (stage 3) showing:
1- Soft tissue thickening
2- Subcutaneous gas
 Necrotizing Fasciitis
• Treatment
1) Emergency debridement
-entire necrotic area should be excised
-wound should be well irrigated
-post debridement, the wound should be kept open & inspected regularly
2) Soft tissue construction-
once all of affected area have been debrided
3) Antibiotic
- Specific ab may be given after result of initial gram stain smear, culture and
sensitivity.
4) Hyperbaric oxygen therapy (recommended for anaerobic organism)
-given aggressively after the first surgical debridement
5)Fluid therapy - to maintain good hydration
6) Analgesic
 Complications:
- Overall mortality is up to 30% from:
• MOF
• Septic shock.
• Toxic shock syndrome (TSS)
- Contributing factors:
* Old age. * DM. * Missed early
diagnosis.
* Trunkal invol. * Anorectal invol.
* Late pres. * Failure after 1st op.
File TM, Tan JS. Group A strept. necrotizing fasciitis. Compr
Ther. 2000;26(2):73-8.
Osteomyelitis
 Osteomyelitis HALLMARK:
• Infection of the bone caused Bone destruction & new
bone formation
by an infecting organisms
Hematogenous Post-traumatic

Acute Subacute Chronic

within 2 weeks >1 month Several
months/ years
 Acute Hematogenous Osteomyelitis

• MORE COMMON in children

– Older children : USUALLY at the metaphysis of growing long bone (prox
tibia, prox/distal femur)
WHY?
• growth plate acts as barrier to spread from metaphysis to epiphysis
• d/t hairpin loop blood vessels in the site -> slow down rate of blood flow

– Infants : risk of epiphyseal extension, joint involvement, growth disturbance

• Immunocompromised adult
– eg: DM, IVDU, due to debilitation
– Normally involves vertebrae but it can be anywhere
 Common organisms

• Staphylococcus aureus (70% of infection)

• H. influenza (in children)
• E. coli*
• Pseudomonas aeruginosa *
• Proteus mirabilis *
• Streptococcus pyogenes * Usual organisms in
• Streptococcus pneumonia Chronic OM
including Staph.
• Salmonella sp. (sickle cell anaemia)
aureus
 Osteomyelitis Organism Table
Age group Most common organisms
Newborns  S. aureus, Enterobacter species, and
(younger than 4 mo) group A and B Streptococcus species

Children  S. aureus, group A Strep sp, Kingella

(aged 4 mo to 4 y) kingae, and Enterobacter sp.

Children, adolescents  S. aureus (80%), group A Strep sp., H.

(aged 4 y to 18 y) influenzae, and Enterobacter sp.

Adult S. Aureus &

occasionally Enterobacter or Strep sp.

Sickle Cell Anemia Patients S. aureus is typically most common,

but Salmonella species is
pathognomonic
 Mechanisms of Spread

1. Hematogenous (originated/transported by
blood)
– Local trauma & bacteremia that leads to susceptibility to bacterial seeding

2. Direct inoculation
– Penetrating injuries
– Surgical contamination
 Pathology
1. Inflammation
Increase intraosseous pressure intense pain  obstruction of blood

2. Suppuration
Pus appears in medulla  spreads along the Volkmann canal towards surface
 forms subperiosteal abscess

3. Necrosis
Compromised blood supply  bone dies  forming sequestra

4. New Bone Formation

Over time, new bone thickens  forms involucrum enclosing infected tissue &
sequestra

5. Resolution
If infection controlled, intraosseous pressure decreases  bone will heal though
still thickened
 Clinical features
Infant
• Failure to thrive
• Drowsy & irritable
• History of birth complication,
umbilical artery
catheterization
• Metaphyseal tenderness,
restricted joint movement
• May or may not have fever
Children Adult
• Severe pain, malaise,
fever • Usually occurs in
• Refuse to use affected vertebrae
limb
• Joint movement is • History of
restricted urological procedure
• Affected limb : local followed by mild
redness, swelling, warm, fever and backache
edema, pus
• h/o skin lesion, injury,
sore throat, ear discharge
On examination:
• pulse >100 (tachycardia) , increased body temperature
• local redness, swelling, warmth and edema
• Limb held still
• Tenderness
• Pain on weight bearing
• Restricted joint movement
 Investigation
Blood
Investigation Result
1. Full blood count WBC 

2. ESR, CRP Increase

3. Blood C&S Organisms cultured

Pus/fluid aspiration
• from subperiosteal abscess / adjacent joint
• Most certain way to confirm clinical diagnosis
• Culture and sensitivity
• Gram stain
 Imaging – Plain x-ray
Acute Osteomyelitis

PLAIN X-RAY 1st week – no abnormal changes

2nd week – rarefaction of the

metaphysis + periosteal new
bone
formation

Healing – sclerosis + thickening

of
the cortex ± sequestra

Delayed / ineffective treatment –

Ragged features of bone
destruction
• Involucrum – new
bone formation

• Sequestrum –
fragment of bone
that has become
necrotic
 Other imaging
• Ultrasonography
– Subperiosteal collection of fluid (early)

• Radionucleotide scan
– Blood flow and cell activity in the involved area

• MRI
– Doubtful diagnosis, suspected infection of axial skeleton
– Extremely sensitive, differentiate between soft tissue infection and
osteomyelitis
 Management PRINCIPLE OF
MX:
• Supportive 1. Rest affected part
– Analgesics, Splintage 2. Provide analgesia
• Antibiotic & general
supportive
– Empirical Abx
measures
– Older children & fit adults: IV 3. Initiate Abx
Flucloxacillin + Fusidic acid (Staph 4. Surgical
infection)  1-2 weeks then oral Abx for debridement (of
3-6 weeks pus & necrotic
– Children under 4 y.o.: 3rd gen tissue)
Cephalosporin (Haemophilus infection)
– Heroin addicts/immunocompromised: 3rd
gen cephalosporin or
Flucloxacilin+gentamycin
 Complications

• Spread to joint causing septic arthritis &

metastatic osteomyelitis
• Growth disturbance due to damaged physis
(shortening / deformity)
• Chronic osteomyelitis
 Subacute Hematogenous Osteomyelitis

• Milder form of acute OM - less virulent

organism or better patient resistance
• Common sites  Distal femur , Proximal &
Distal Tibia
• Usually affecting children or adolescent
• X-ray finding – Brodie’s abscess (small oval
cavity surrounded by sclerotic bone)
• Mx - drainage & Abx
Subacute osteomyelitis
• Brodie’s abscess

• Oval lytic lesion

 Chronic Osteomyelitis
• Sequel of acute hematogenous, post-traumatic,
post-op
• Presents with:
– Recurrence of infection - pain, fever, redness and tenderness
– Discharging sinus
– Seropurulent discharge
Chronic
osteomyelitis

• Plain X-ray

• Bone rarefaction
(porous)
surrounded by
sclerosis +/-
sequestra
 Management
• Treatment depends on the frequency of relapsing
flare-ups, seldom -> conservative
• Antibiotics - Fuscidic acid / cephalosporins
• Sequestrectomy (only if sequestrum is
radiologically visible and surgically accessible)
• Frequently recurring : excise the infected bone ±
devitalized segment of bone, then close the gap
by transporting a viable segment from the
remaining diaphysis (Ilizarov method)
 Post-traumatic/Post-op osteomyelitis
• Most common in adults
• Complication of open
fracture
• Common organism
– Staph. Aureus (most common)
– E. coli
– Proteus mirabilis
– Pseudomonas aeruginosa
Risk Factors for post-op OM :
1. Chronic disease
2. Multiple ops at the same time
3. Difficult/long ops
4. Tight dressings
5. Old age
6. immunosuppressed
 Clinical features

• Fever
• Pain
• Swelling over the fracture
site
• Wound is inflamed
with seropurulent
discharge
 Investigation

Blood
Investigation Result
1. Full blood count WBC 

2. ESR, CRP Increased

Wound swab
-culture for organism
-test for antibiotic sensitivity
 Management
Prophylaxis
• Thorough cleansing and debridement of open
fractures
• Leaving wound open for drainage
• Stabilisation of fracture
• Antibiotics: flucloxacilin + benzylpenicillin
for 6hrly for 48 hours
 Management
• Regular dressing and repeated removal of
dead and infected tissue
• Stable implants left in place until fracture
united
• External fixation- accessible for dressing &
debridement (for unstable fracture)
• If fail, management of chronic osteomyelitis
SEPTIC ARTHRITIS
 Introduction
• Septic arthritis is an inflammation of a joint
• It is usually due to bacterial infection (usually
Staphylococcus aureus)
• It may be seen at any age
• In children, it occurs most often in those younger
than 3 years
• Can affect any joint - commonly affect the hip in
children and the knee in adults
 Route of spread

• Hematogenous (most common)

• Spread from contiguous soft tissue
infection
• Direct inoculation (penetrating injury)
• Spread from metaphyseal osteomyelitis
where the metaphyseal is intra-
articular
Pathologically : Organism (usually Staphylococcus
aureus) reaches joint by haematogenous/local
spread from femoral osteomyelitis

Cartilagenous femoral head liable to be destroyed

by proteolytic enzymes of bacteria and pus
 Risk factors
• Artificial joint implants
• Bacterial infection elsewhere in the body
• Chronic illness or disease (eg diabetes,
rheumatoid arthritis, and sickle cell disease)
• Intravenous (IV) or injection drug use
• Drugs that suppress the immune system
• Recent joint trauma
• Recent joint surgery
 Causative Organisms
Neonates Child 1-4 > 4 years Adults
+ years
< 1 year
S. aureus S. aureus S. aureus S. aureus

Group B H. Streptococc Streptococc

Streptococc influenzae us i (A, B, C, G)
us pyogenes

Since the introduction of the HiB vaccine, the incidence

of Haemophilus
Infections has dropped dramatically
• In early stage, there is an acute synovitis with
a purulent joint effusion
• Soon, the articular cartilage is attacked by
bacterial and cellular enzymes
• If the infection is not arrested, the cartilage
may be completely destroyed
• Healing then leads to bony ankylosis
 Clinical features
• It depends on the age
• Typical features : joint swelling and intense
joint pain (diffused pain – widespread)
Clinical features in newborns and infants
(the emphasis is on septicaemia rather than joint pain)

• Pain - cries when infected joint is moved

(tenderness maximal over hip) – cries during
diaper changing
• Pseudoparalysis - unable to move the limb with
the infected joint
• Fever + sign of inflammation (absent in neonates
– blood tests often normal)
• Irritability
• Lethargy
• Refuse feeding
 Clinical features in children and
adults

• Pseudoparalysis - inability to move the

limb with the infected joint
• Intense joint pain
• Joint swelling
• Joint redness
• Low grade fever
 Investigations

1. Blood tests
• FBC – increase in WBC
• ESR/CRP - increase
• Blood culture – guides for antibiotic choices

2. Culture and sensitivity of joint aspirates

(under GA) – guides for antibiotic choices
3. Radiological investigation

• Plain radiography of affected joint

• Ultrasound – joint effusion
• Bone scans – T99, Indium and gallium
• Radionuclide imaging and MRI – detecting
signs in difficult site (sternoclavicular and sacroiliac
joints)
 Plain radiography
• During first 2 weeks
- Soft tissue swelling
- Widening of the joint space (due to the effusion)
- Periarticular osteoporosis

• Later (more than 2 weeks) articular cartilage is

attacked, the joint space is narrowed

• In advanced case, there are signs of bone destruction

During the first 2 weeks, widening of the medial joint space is
noted in the right hip as compared to the left hip (arrows)
If more than 2 weeks, articular cartilage is attacked - the joint
space is narrowed
 Treatment

1. Medical
• Supportive
- Analgesics
- Hydration
- Immobilisation (splint/traction) if needed

• Antibiotics

2. Surgical

3. Follow up
The first priority is to aspirate the joint and
examine the fluid
 Antibiotics
• Anti-staphylococcal antibiotic
1. First line
• Cloxacillin – given intravenously, 1-2g 6 hourly (until ESR or
CRP is normalized, CRP is more sensitive than ESR)
• Fucidic acid – 500mg orally, 8 hourly (provided parents are
reliable, and antibiotics does not cause GI disturbances that
would interfere with absorption)
2. Second line
• Vancomycin

• Anti-streptococcal antibiotics
1. Benzylpenicillin
 Surgical managements
• Perform repeated percutaneous joint aspirations
(only if easily accessible peripheral joint, clinical course <6days and osteomyelitis is
ruled out)

• If condition fails to improve, perform open drainage in OT

Indications :
- Hip and shoulder joints
- Peripheral joints that do not respond to percutaneous aspiration
- Patients who are systemically ill
- Suspected organisms (S. aureus/gram –ve) produce cartilage damaging
enzymes
(Continue open drainage)

Role of open drainage :

• Eradicate and dilute bacteria inoculum
• Destructive enzymes from immune response
• Decompress
• Excision nonviable tissues

• Apply traction on hip or splint until infection

resolved
- If instability is suspected, immobilize patient for longer
period
Follow up (at least up to 1 year after
surgery)
• Assess joint function

• Plain radiography – to ensure no

radiographic evidence of loss of joint space,
avascular necrosis of epiphysis, joint
instability, damage to growth plate
 Complications
• Epiphyseal destruction
• Growth disturbance
- Physeal damage result in shortening or deformity
• Dislocation of the joint
- Due to tense effusion
• Ankylosis
- If articular cartilage is eroded, healing may lead to
ankylosis