Infections of Bones CHAPT

oponl
and Joints 29
Acute and Chronic Osteomyelitis
DEFINITION
Infection of bone and bone marrow.

ICLASSIFICATION
On the basis of
A. Route of spread
1. Direct: Open
injuries/adjacent infective foci (E.g., osteomyelitis of mastoid due to
chronic suppurative otitis media, Garre's osteomyelitis due dental caries)
2. Indirect/hematogenous to
B. Type of infection
1. Pyogenic
2. Tubercular
3. Fungal
C. Duration of infection
1. Acute: Less than 6 weeks
2. Primary subacute: Within 6-12 weeks
Brodie's abscess
Sclerosing osteomyelitis of Garre's
3. Chronic: Greater than 12 weeks.

PREDISPOSING FACTORS
1. Infants and children are more prone: Probably due to lesser immunity
2. Boys more prone than girls (4:1): ?Boys more to trauma
prone
3. Poor nourishment: Poor immunity
4. Poor host response
5. Sickle cell anemia: Leads pro
to bony infarcts and microaerophilic environ emia.
motes growth of bacteriä. Salmonella osteonyelitis is common in Sickle ceu
6. Trauma to the metaphysis.
 Infections of Bones and Joints 289

Acute Bacterial (Pyogenic) Osteomyelitis

Morison aphorism (1935): Nontraumatic pain and swelling at the end of a long bone
Rutherford should be taken as acute osteomyelitis unless proved otherwise
in a child s
(metaphysis)

JETIOLOGY

The
c o m m o n
bacteria that cause acute osteomyelitis (OM) are
Staphylococcus aureuS: Most conmmon organism to cause pyogenic OM
Streptococcuspyogenes
Pneumococci

,Haemophilus: 6 months-6 year child

Pseudomonas aeruginosa: In IV drug abusers, immunocompromised
Salmonella: Multifocal OM, patients with sickle cell anemia
, Brucella abortus/suis: Due to drinking of unpasteurised milk/in direct contact with
infected bovine/pig. Commonly, Brucella osteomyelitis causes vertebral osteomyelitis and
mimics Pott's spine.

PATHOGENESIS OF ACUTE HEMATOGENOUS

PYOGENIC OSTEOMYELITIS
There three stages in
Ine most common site for hematogenous osteomyelitis is metaphysis.
are

the development of pyogenicosteomyelitis.

1.Stage ofIntramedullary abscess
2.Stage of Subperiosteal abscess formation
6.
Stage of Sequestration and involucrum
Ajlowchart (page 291) summarizes the pathogenesis of osteomyelitis (Flouchart 29. 1).

29.1A D)
Stage ofIntramedullary intraosseous abscess (Figs.
to

bacteria tend to settle down in the meta-

nce there is bacteremia reaching the bone, the
physeal region of the bone due to several reasons:
Hairpin loop structure of the "metaphyseal capillaries": Leads to blood stagrnation

and consequent bacterial proliferation

discontinuous endothelium at the tip
apid growth in metaphysis leads to vessels with bacteremia
bessel facilitating passage of bacteria into bone during cell turnover with more cell
etaphysis is m o r e metabolically active: Leads to high
debris available for bacterial activity
telative lack ofphagocytes in the metaphysis
environmen, and multiplication results in
nce, local bacterial stagnation, favorable destruction of bac
response from the host defense system leading to widespread
e ho s t cells and a consequent intramedullary abscess formation.

Fate of intramed in various age groups.

fants: P edullary abscess with respect to growth plate (physis)
from metaphysis which penetrate physis and can
physis as there are vessels
each the ioi
ach penetrate
joint via
Pus cannepiphysis.
Children: ocannot penetrate the physis there is no vascular
connection and physis is quite thick
Adults: p e n e t r a t e the
as

it is very thin after growth

is over and pus can reach the joint
physis as
290 Manipal Manual of Orthopaedics

Growth plate -

Early infection

Hair pin bend -

vessels Intramedullary
abscess
Periosteum
Periosteum

A B

Pressure of the
intraosseous
abscess
Over the cortex

D
C
29.1A to D: Stage of intraosseous abscess
Figs.

2. Stage of Subperiosteal abscess formation (Figs. 29.2A and B)

2.
toward the adjacent cortex and causes
Once the abscess is formed, it usually spreads
necrosis of the cortex due to
Pressure over the cortex (Figs. 29.1C and D)
the cortex blood
Thrombosis of the medullary and periosteal vessels jeopardizing
supply and further released
Thus, the abscess underlies the periosteum after eroding the cortex
into the subcutaneous plane after eroding
the periosteum (Figs. 29.2A and B).
3. Stage of Sequestration and sinus formation (Fig. 29.3) reaches into
The subperiosteal abscess the periosteum,
perforates the subcutaneo
the skin surface via a sinus.
plane and further bursts onto
The cortical bone with impaired blood supply undergoes sequestration
The new bone starts forming around the sequestrum known as the involucrun

Skin

Sub-
periosteal
Abscess in
abscess
subcutaneous

Periosteal plane
elevation and
A reaction B
Figs. 29.2A and B: Stage of subperiosteal abscesS
 Infections of Bones and Joints
291

I MPORTANT
Possible route of
metaphyseal
intraosseous abscess spread
Subperiosteal, and then to the soft
tissues
Sequestrum formation Into the growth plate
Sinus Into the diaphysis
Into the Joint
(Septic arthritis)
Cortical thickening and Septic arthritis
following
irregularity osteomyelitis is common metaphyseal
in areas where
there is
'intracapsular
Sclerosed cavity with the subperiosteal abscessmetaphysis', Once
pus and infected
bursts outside
the
granulation tissue
intracapsular metaphysis, the abscess
directly opensinto the joint.
Fia. 29.3: Locationof intra-articular
Stages of sequestration and sinus 1. Proximal humerus metaphysis:
formation 2. Radial head
3. Neck femur

Flowchart 29.1: Flowchart

showing the process of
osteomyelitis
Bacteremia Bacteria into metaphysis

Host immune Local bacterial proliferation

system response
Exudation, necrosis

Acute metaphyseal intraosseous

abscess formation
- Abscess causes pressure over the
adjacent cortex 'pressure necrosis'
-

Thrombosis of medullary and periosteal

vessels jeopardizing cortical vascularity

Cortical necrosis

Pus escapes into

Necrosed dead bone
becomes 'sequestrum Subperiosteal region
'subperiostealabscess

New bone formation Periosteal reaction

around sequestrumm

nvolucrum forms with cloacae. Pus escapes into

Cloacae lets chronic medullary subcutaneous plane
pus and small
sequestrum
escape to surface
Via sinus tracts/directly. Sinus formation
292 Manipal Manual of Orthopaedics

ICLINICAL FEATURES OF ACUTE OSTEOMYELITIs

1. Neonates and Infants
Refusal to feed, restless
Fever/hypothernmia; often dehydrated
Pseudoparalysis of the affected limb
2. Children
High-grade fever; often dehydrated
Severe pain over the atfected part
Swelling and bonytenderness over the metaphyseal area
Skin may show sings of inflammation
Severely restricted movement at the joint Pseudoparalysis
.Mild joint effusion (sympathetic)
3. AdulIts

Fever
Pain, swelling, and tenderness over the metaphysis
Painful range of movement due to muscle spasm.
DIFFERENTIAL DIAGNOSIS
Ewing's sarcoma: In children, diaphyseal involvement
Septic arthritis: Joint movements are extremely painful
Scurvy Multiple areas of swelling and tenderness over many bones.

INVESTIGATIONS
KComplete blood picture (CBP): Elevated total counts, Neutrophilia
2 Elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); Elevalru
3. Blood culture
4. Culture from local site if sinus already formed/subcutaneous abscess
5. X-ray of the affected bone (Fig. 29.4)
Normal till 10-14 days (Hence, no role of X-rays till 2 weeks in acute osteomyeinns
After 2-3 weeks: Periosteal reaction, localized rarefaction
6. Tc99 bone scan
Useful in multifocal cases of
osteomyelitis or within 2 weeks when X-rays a infec
andintea
Sensitive but not specific as it can be
positive (hot spot) in trauma, tumoty*
morespecihc
tions. However, leukocyte labeled Indium-111 scan or Gallium scansare
7. Magnetic resonance imaging (MRI) (Fig. 29.5)
Most sensitiveand specific
. Reveals earliest medullary abscess
stigation
8. Aspiration of intraosseous pus with wide bore needle: Confirmatory mve
T o be sent for Gram stain and
cultuure/sensitivity (C/S)

twerh
 Infections of Bones and Joints 293

Fig. 29.4: X-ray shows lytic area in proximal tibial

Fig. 29.5: MRI of tibia shows intramedullary
metaphysis (left image) and periosteal reaction abscess
(arrow

TREATMENT
The treatment of acute osteomyelitis depends upon the time of clinical presentation (within or
after 48-72 hours)
1. Clinical presentation within 48-72 hours: Initiate only medical treatment. Surgical treat
ment to be given if there is NO response to the medical treatment even after next 2-3
days
2. Clinical presentation after 48-72 hours: Initiate surgical treatment followed by medical
treatment
Flowchart 29.2 illustrates the treatment of chronic osteomyelitis.

Flowchart 29.2: The treatment of the acute osteomyelitis

Onset of acuteosteomyelitis

<48-72 hours >48-72hours

Supportive Broad spectrum antibiotics Surgical Supportive

treatment covering 'Gram-positive and decompression of treatment
Analgesics gram-negative' bacterias intraosseous abscess - Analgesics

Antipyretics followed by specific antibiotic

- Antipyretics

Splints/tractions
IV luids Continue broad
Splints/tractions
- IV fluids
spectrum antibiotics
Daily Follow up
- Clinical (for gram+,
gram-bacteria) followed
- Serological (CRP)
by specific antibiotic

If clinical features and serology

Continue antibiotic
x6-8weeks
Improve Worsen/fails to
improve
Continue supportive
and antibiotic treatment
x6-8 weeks
ovenkd
 wmurohc
ors
1 6 we clis
294 Manipal Manual of Orthopaedics

General supportive treatment: Start in all the patients

A.
Analgesics: Forpain relief
medications
Antipyretics and anti inflammatory
Fdema control: Limb elevation and magnesium sulfate dressings
Intravenous (1V) fluids: For treating dehydration
and contractures
Tractions/splint: For prevention of deformity
B. Medical treatment: Patient is started on broad spectrum IV antibiotics covering
gram
positive and gram-negative microbes (E.g., Vancomycin +Cefipime/ Linezolid +Cefinimo
Flucloxacillin + 3rd gen Cephalosporin) |Nte: source f this info is from BMJ best ctice

2018].
Once the culture-sensitivity of pus is ready, the patient is started on specific antibiotics
Duration of antibiotics: 2-3 weeks ofIV antibiotic+ 4-6 weeks of oral antibiotic,
If the patient's clinical features improve, then antibiotic is continued for the above-said
duration.
However, if there is no improvement in clinical features or there is worsening; the surgical
treatment is opted.
C. Surgical treatment: Indications
1. No clinical improvement/worsening in symptoms after antibiotic is started
2. Presentation after 48-72 hours as intramedullary abscess does not respond to antibiot
ics alone.
T h e surgery involves "opening of the cortical window" in the cortex to allow the
drainage of the intramedullary pus (Fig. 29.6).
The cavity can be filled by antibiotic-laden bone cement for local release of antbi
otic which are removed after 6-8 weeks.
The antibiotic treatment is continued as discussed above for 6-8 weeks

Fig. 29.6: Left image shows penetrated cortex with pus in vicinity whereas right image sno
"cortical window opening

ICOMPLICATIONS
1. Chronic osteomyelitis.
2. Growth plate damage: Results in deformity, limb length discrepancy
3. Septicemia
4. Pathological fracture
5. Septic arthritis: More commønwith'intra-articular metaphysis such as proxima
radial head and neck femur.
 uoabuy
Infections of Bones and Joints 295

Chronic Osteomyelitis (wtur

IDEFINITION
drrcdoprnp Tu
Chronic osteomyelitis is the persistent bone and bone marrow
infection characterized by the
presence of an infected cavity with the sequestrum, the involucrum, and a discharging sinus.

PREDISPOSING FACTORS
Untreated/inadequately treated acute osteomyelitis
Compromised local host defenses, poor local vascularity
Bacteria covered in glycocalyx:
protects it from antibiotics and immune cells
Compromised immune system: Old, debilitated patients, diabetics, malnutrition
Local trauma: Open fractures

Why does osteomyelitis become chronic and is difficult to treat?

Bacteria survive intracellularly in the osteoblasts.
Bacteria undergo phenotypic alteration in the
antimicrobials
osteoblast which renders it more resistant to
Potential protective proteolytic activity is inhibited in the
Bacterial adherence to collagen
presence of infection.
Dead bone
(sequestrum) cannot be resorbed
Rigid bony cavities cannot collapse

PATHOPHYSIOLOGY OF CHRONIC OSTEOMYELITIS

The chronic medullary infection leads to thronmbosis of blood vessels and periosteal stripping
results in loss of blood supply to the cortex
leading to destruction and devitalization of bone.
This causes the
separation of dead cortical piece as sequestrum' which is surrounded by pus
and
infected granulation tissue. Sequestra acts as substrate for bacterial adhesion and ensures
the persistent infection. There is a sinus tract formation' trom the bone surface to the skin
O let the pus and smaller
pieces of sequestrum let out of the infected cavity. Sinus seals off
0T lew
weeks-months to open later sometime again. In response to the loss ot cortical bone
Sequestrum, the healing response of the body results in a reactive periosteal new bone
oration around the sequestrum known as involucrum. The presence of involucrum
hstrength to the weakened bone as there is loss of cortical bony support as sequestrum.
Vlucrum has small fenestrations cloacae to let the pus and sequestrum get discharged
the surface
bone becomes directly
or via sinus tract. The entire infected medullary cavitatory area in the
heavil o
e s avily sclerosed in an attempt to wall off the infected cavity from the normal
bone. This
sclerosis o
Sclerosis cuts offthe blood supply to the cavity wlhich resules in persistent intection.
296 Manipal Manual of Orthopaedics

Flowchart 29.3 below summarizes the pathology of chronic osteomyelitis.

Flowchart 29.3: Pathology of chronic osteomyelitis

Intramedullary infection
thrombosis of blood vessels

Loss of Cortical blood supply

Chronic infected granulation tissue with pus in the cavity

Infected, dead bone known as Sequestrum Formation of sinus tract to the skin to
surrounded by infected granulation tissues and pus let the pus and sequestrum vent out

Reactive new bone formation around

sequestrum (Involucrum)

ICLINICAL FEATURES Types of sequestrum

Cortical: Flat and serrated
Insidious onset (hematogenous). vory: Syphlitic
Sometimes h/o trauma
Sandy/rice grain: Tubercular osteomyelitis
Pain and swelling over the affected bone
Feathery: In TB of ribs
H/Orepeatedly discharging sinus (Fig. 29.7) Black: Fungal osteomyelitis
H/O discharging bony spiculesthrough Ring/Annular: Around amputation stump/
pin tracts
sinus
Diaphyseal: Seen in children wherein
Examination reveals whole diaphysis becomes a sequestrum
A. Inspection
Often multiple scars over the limb (due to
sinus, surgery, old wounds)
Discharging sinus t
Muscle wasting, deformity
B. Palpation

Bony thickening, irregularity, and tenderness

Presence of a discharging sinus (single or mul-
tiple) over the limb which is fixed to the under
lying bone
Discharging sinus
C. Other features: Fig. 29.7:

Joint stiffness
Limb length discrepancy plae
Regional Lymph nodes may be enlarged

pV
 Infections of Bones and Joints
297
INVESTIGATIONS

Plain X-ray: Quite diagnostic (Fig. 29.8)

Cortical thickening and irregularity
Presence of sequestrum: Dense, irregular and separate
piece on Xray

Involucrum
Single/multiple cavities

Sometimes other features

.Pathologicalfractures
Nonunion or malunion of the fracture
Fig. 29.8: Plain X-ray of the arm
2 CT scan (Fig. 29.9A)
showing chronic osteomyelitis
To detect sequestrum
of humerus: Sequestrum (yellow
3. MRI arrow): Involucrum (blue arrow)
Only if there is abscess collection in tissue planes
ua tming d e not
Sinogram (Fig. 29.9B).
.To track the sinus tract pathway
It can also be combined with CT scan as CT
sinogram

O
5. Culture and sensitivity (C/s)
Purulent material from the sinus opening is
sent for C/S.

ITREATMENT
The treatnment of the chronic osteomyelitis is
"Essentially Surgical" followed by medical.
B
Figs. 29.9A and B: Computed tomography
The principles of treatment are (Flowchart 29.4)
(CT) scan shows sequestrum (A) and
A. Treatment of the dead bone and tissues sinogram shows sinus tract (B)
B. Treatment of the dead space

Flowchart 29.4: Flowchart for the treatment of the chronic osteomyelitis

Principle of Sinus tract excision

Treatment of chronic osteomyelitis 2. Sequestrectomy
3. Saucerization
4. Curettage
5. Antibiotic laden bone cement application in the cavity
Treatment of the dead tissue 6. Prolonged antibiotics (6-12 weeks)
(bone and soft tissue) and infection 7 . Sometimes. Ilizarov method is used to treat
chronic osteomyelitis (especially with
nonunion/shortening etc) with excision of
infected bone and reconstruction of bone
Treatment of the dead space Fill the curetted, saucerized cavity with
After local infection is controlled)
1.Cancellous bone graft OR
Free Vascular bone graft
2 Soft tissue defect closure byy
Myofasciocutaneous flap transfer
 298 Manipal Manual of Orthopaedics

A. Treatment of the dead tissue and bone involves several steps

1. Sinus tractexcision
The infected sinus tract is excised.
2. Sequestrectomy (Fig. 29.10)
The sequestrum is rem ved once adequate
involucrum is formed (source ofpersistent infec-
tion is removed).
3. Saucerization (Fig. 29.11)
The pitcher-shaped infected cavity is converted
into a saucer-shaped cavity by deroofing the cav-
ity. This ensures that the whole sclerosed cavity
is no more a narrow mouth cavity where infec- Fig. 29.10: Sequestrum
removed
tion and purulent material can get collected;
rather it drains via a big opening.
Note: The saucerization is done only once
"adequate involucrum" is formed around the
sequestered bone or else it increases the risk of
pathological fracture as saucerization involves
removal of part of normal bone and involucrum'
which results in weakening of bone.
4. Curettage of cavity
The entire wall of the cavity is curetted so that
the infected granulation tissue and purulent
Fig. 29.11: Saucerized cavity of
material are completely removed and margins of
chronic osteomyelitis
cavity reveal fresh bleeding. This ensures robust
blood supply to the infected cavity which carries immune cells and delivers systemri
antibiotics to the cavity which helps in fighting residual infection in the cavity.
5. Antibiotic-impregnated bone cement may be kept as a bead in the cavity. This ensue
the local deliveryof the antibiotic for prolong periodof4-6veeks. Usually Vancom
Gentamycin is used in Bone cement.
6-8weeks later, the beads are removed (Figs. 29.12A to E).
for a
After the surgical debridement, the culture-specific antibiotics are cOne
period of 2-3 months and rarely, upto 4-6 months.
nonunion.
6. Resistant hone infection with other associated
complications sucn a gment is
shortening, deformity are best treated with llizarov method. Here, the dead seg
resected and viable segment is
B.
transported.
Treatment of the dead space: The dead
a n d remains a

space could result reinlecto

in
potential risk factor for the pathological factór
Hence, the space is filled up with
(Papineau technique)
oal 1. Delayed Open cancellous Bone
grafting after 2-3 weeks. also
an

is
the cavity the local graft
once
infection is controlled. Free vascularized bo
option.
2. flaps
Filling/covering the dead space by myocutaneous flaps/fasciocutaneo
 Infections of Bones and
Joints
299

C
. D

pMMA
Figs. 29.12A to E: Images
of Bone cement with showing the preparation
gentamycin. (A) Bone cement
(PMMA, polymethylmethacrylate) with liquid
tor.(B) Bone cement mixed with activator activa
Bone cement rolled into semisolid liquid. (C)
beads. (D) Beads
are rolled over the
stainless steel wires and let hard-
ened. (E) Beads are
applied over the infected area

IcOMPLICATIONS OF CHRONIC OSTEOMYELITIS

Recurrences after the treatment
2. Pathological fractures

Limb length discrepane

it g n discrepancy: Observed
results in in children due to damage to
growth plate. Mostly
shortening
due to e n i n g due
c
stimulation
to damage to physis. However, rarely there can be lengthening
ing could of phy
hysis due to hyperemia in adjacent infected area. In adults, shorten
result edue
Deformis
ofDeformity:
grov uDuec toto toassymetric
bone
loss,growth
pathological
plate fracture
(physis) destruction. This results in arrest
in one
Tesulting in deformity.
a
part of physi: whereas other part of physis continues to grow normally
300 Manipal Manual of Orthopaedics

5 Sinus tract malignancy: With sinus

persisting for many years, it could result in
cell carcinoma of the tract squ1ame.
nous
6. Amyloidosis: After many years of chronic osteomyelitis
7. Rarely, Septicemia
8 Joint stiffness: Due to muscle and other soft tissue contracture.
result from septic arthritis.
Sometime, it could al

Brodie's Abscess and Garre's

Sclerosing
Osteomyelitis
BRODIE'S ABSCESS
Definition
It is
primary subacute osteomyelitis of
a

of organism or hematogenous origin.

strong host immune response.
It occurs due to low virulence
Most Common Location
Proximal tibial metaphysis.
Sometimes in distal tibia, fibula, distal
radius, carpal or tarsal bones.
Etiology
Usually any age
Staphylococcus aureus (usually of low virulence or
strong host immunity and respponse.
Clinical Features
Pain, swelling at
the upper end of leg
Night pain
Bony tenderness at the upper end of
MildMild swelling tibia
Usually nomal novements.

Investigations
1. Raised ESR
2. X-ray: Lytic cavitatory lesion
reaction is observed. surrounded by a dense sclerotic rim of bone. iosteal

3 MRI: Lytic lesion with

bone abscess cavit thi 'penumbra sign' (a rim of vascularind nn ticsue arounu