INFECTION

dr. Ronald V Munthe SpOT

Infection
Is a condition in which pathogenic
organism multiply and spread
within the body tissues

Classical sign : Kalor, Rubor, Dolor, Tumor, LOF

Stab wound, operation,

open fracture

Blood stream (hematogen)

Nose, mouth, bowel, GU tract

Directly

Indirectly
type of invader
the site of infection
the host response

Acute Pyogenic
Infection

Sub-acute Phase
Chronic

Pus
(defunct leucocytes, dead bacteria
tissue debris)

Granulomatous
Reaction

Granuloma
(lymphocyte, macrophage
giant cell)

Host susceptibility
Local Factor:
Trauma
Poor circulation
Sensiblity
Foreign body (+)
Chronic bone or
joint disease

Systemic factor
Malnutrition
Diabetes
Imunitas
Debility

Acute Haematogenous Osteomyelitis

Acute Haematogenous Osteomyelitis

Common in children
Adults with special condition
diabetes, immunocompromised, malnutrition, drug user

Post-traumatic event
haematomes, fluid collection

Acute Haematogenous Osteomyelitis

Gram +

Gram -

Staphylococcus Aureus

Haemophylus Influenza

Streptococcus Pyogenes

E. Coli

Streptococcus Pneumonia

Pseudomonas Aerogenosa
Proteus Miriabilis
Bacteroides Fragilis

Acute Haematogenous Osteomyelitis

Characteristic Pattern
Inflammation
Suppuration
Necrosis
New Bone Formation
Resolution or
Intractable chronicity

Acute Haematogenous Osteomyelitis

Inflammation
Vascular congestion
exudation of fluid

leucocyte infiltration

intra-osseus pressure

PAIN

Acute Haematogenous Osteomyelitis

Suppuration

Acute Haematogenous Osteomyelitis

Suppuration

Acute Haematogenous Osteomyelitis

Necrosis

intra-osseus pressure

Periosteal Stripping

vascular stasis, thrombosis

due to pus

Compromise blood supply

+
Bacterial toxins

Bone death

sequestra

Acute Haematogenous Osteomyelitis

New Bone Formation

Stripped periosteum

Deep layer new bone formation

Involucrum
Enclose the infected bone
& sequestra

Patogenesis (4)
Setelah 1 minggu terjadi nekrosis tulang
Sequester.
Setelah 2 minggu terbentuk tulang baru
dari periosteum yang terangkat
involucrum.
Pus mencari jalan keluar membuat lubang
yang disebut cloaca/fistel

Acute Haematogenous Osteomyelitis

Resolution or
Intractable Chronicity

Healing

Antibiotics & Intraosseus decompression

Remodelling

Normal bone contour

Acute Haematogenous Osteomyelitis

Clinical Features
Look

Feel

Swelling

Pain

Hyperaemia

Febris

Pus discharge

Fluctuation

Lymphadenopati

Tachicardia

History of infection

Tenderness

Move

Refuse to use affected limb

Not appear in early antibiotocs treatment

Diagnostic Imaging

Diagnostic
Imaging

X-Rays

No abnormalities
Displacement
Combination
fat plane
Patchy
rarefication
Extra cortical outline
Osteoporotic
Haematoma Periosteal new bone
metaphysis
Inc. dense
swelling

1-2 days

10-14 days

>21 days

Diagnostic
Imaging

Diagnostic
Imaging

USG

Radioscintigraphy
99mTc-HDP

67Ga-citrate or 111 ln

MRI & CT

Detect fluid collection

Increased activity in both phase

Sensitive but not spesific

Sensitive
Differentiate
Soft tissue infection & Osteomyeliti

Diagnostic
Imaging

Diagnostic
Imaging

The most certain way to confirm

the clinical diagnosis
is to aspirate pus from
the metaphyseal subperiosteal
abscess or the adjacent joint
Pus Bacteroidal examination
&
Antibiotics sensitivity

Laboratory

White cell count

C-Reactive Protein
ESR
Blood Culture

Differential Diagnose
Cellulitis
Streptococcal Necrotizing Myositis
Acute Suppurative Arthritis
Acute Rheumatism

Treatment

If osteomyelitis is suspected on clinical

grounds,
blood and fluid samples should be taken
and then
treatment started immediately without
waiting
for final confirmation of the diagnosis

Treatment Principles

Provide analgesia + Fluid Therapy

Rest affected part (imobilisasi)
Identify organism and give antibiotic
Pus evacuation and necrotic tissue
Stabilize bone if it has fractured

Treatment

Supportive Treatment
Splintage
Antibiotic Therapy
Surgical Drainage

Treatment

Supportive Treatment

Analgesic

Septicaemia & Fever

Dehydration

Treatment

Antibiotic Therapy
the prompt administration
of antibiotics is so vital, that treatment
should not await the result

Take the best guest

patient's age, general state of resistance, renal function,

degree of toxaemia and previous history of allergy
Must be taken into account

Treatment

Antibiotic Therapy

I.V

(1-2 weeks)

Adults

flucloxacillin & fusidic acid

Staphylococcal
Oral

Children

(3-6 weeks)

I.V

Cephalosporin
(cefuroxime / cefotaxime)

Oral

Amoxyclav

Haemophylus

Treatment

Surgical Drainage
if the clinical features do not
improve within 36 hours of starting treatment, or
even
before that if there are signs of deep pus (swelling,
oedema, fluctuation), and most certainly if pus is
aspirated,
the abscess should be drained by open operation
generalintramedullary
anaesthesiaabscess
if there under
is an extensive
drainage can be better achieved
by cutting a small window in the cortex

Complication

Metastatic Infection
Suppurative Arthritis
Altered Bone Growth
Chronic Osteomyelitis

Sub-Acute Haematogenous
Osteomyelitis

presumably due to
the organism being less virulent or
the patient more resistant (or both)

Sub-Acute Haematogenous Osteomyelitis

Typically there is a well-defined cavity in

cancellous bone, containing glairy seropurulent
fluid
The cavity is lined by granulation tissue
containing a
mixture of acute and chronic inflammatory
cells
The surrounding bone trabeculae are often
thickened

Sub-Acute Haematogenous Osteomyelitis

Clinical Features
Pain near one of the larger joints
for several weeks or even months
May have a limp and often there is
slight swelling, muscle wasting and local
tenderness.
The temperature is usually normal and there is little
to
suggest an infection.

Sub-Acute Haematogenous Osteomyelitis

Imaging
The typical radiographic lesion is a circumscribed,
round or oval cavity 1-2 cm in diameter,
most often it is seen
in the tibial or femoral metaphysis

Sometimes the 'cavity' is surrounded by a

halo of sclerosis, the classic Brodie's

abscess
The radioisotope scan shows
markedly increased activity

Sub-Acute Haematogenous Osteomyelitis

Sub-Acute Haematogenous Osteomyelitis

The clinical and x-ray appearances

may resemble those
of an osteoid osteoma

Biopsy is a gold standard for diagnosis

If fluid is encountered,
it should be sent for bacteriological culture

Sub-Acute Haematogenous Osteomyelitis

Treatment
Conservative
immobilization and antibiotics
(flucloxacillin and fusidic acid) for 6
weeks usually result in healing

Curettage is also indicated

if the x-ray shows that there is no
healing
after conservative treatment

Chronic Osteomyelitis

Chronic Osteomyelitis

dreaded sequel to
unresolved acute haematogenous
osteomyelitis

The usual organisms

(and with time there is always a mixed infection)
are Staph, aureus. E. coli. S. pyogenes.
Proteus and Pseudomonas

Chronic Osteomyelitis

Sequestra
Pus

Vascular Tissue
Sclerotic Area

Sequestra & Foreign implant act as substrate for bacterial adhesion

Chronic Osteomyelitis

Clinical Features
The patient presents because
pain, pyrexia, redness and
tenderness have recurred

(a 'flare')
or with a discharging sinus

Chronic Osteomyelitis

Laboratory
During acute flares
the ESR and blood white cell count
may be increased, these non-specific signs are
helpful
in assessing the progress of bone infection
but they are not diagnostic
Antistaphylococcal antibody titres may be
elevated
a valuable sign in the diagnosis of hidden
infections and in tracking progress to recovery

Chronic Osteomyelitis

Treatment
Antibiotics

Seldom eradicate by antibiotics alone

Stop the spreading

Control the acute flares

Choice depends on bacteriological studies

Capable of penetrating sclerotic bone
Non-toxic with long-term use

Chronic Osteomyelitis

Treatment
Local Treatment
Sinus dressing
Colostomy paste
Incission & Drainage for acute abcess

Chronic Osteomyelitis

Treatment
Significant symptoms
Clear evidence of a sequestrum
or dead bone
All infected soft tissue and
all dead or devitalized bone

Operation
Excised

Dead material can be identified by the preoperative injection

of sulphan blue which stains all living tissues
green, leaving dead material unstained

Chronic Osteomyelitis

Treatment

Chronic Osteomyelitis

Treatment
Papineau Technique
Fill completely the dead space left after excision of necrotic
tissue with
living or potentially living material
Cancellous bone graft
(autogenous)
Antobiotic

Muscle-flap transfer

+
Fibrin sealant
Split skin graft

Post Traumatic Osteomyelitis

Common in adults

The combination of tissue injury, vascular damage,

oedema, haematoma, dead fragments and
an open pathway to the atmosphere
Staph. Aureus

Feverish and develops pain and

swelling over the fracture site, the wound is
inflamed
and there may be a seropurulent discharge

Treatment : debridement, antibiotics, delayed

wound closure

Post Operative Osteomyelitis

The true incidence is probably around 5%

considerably greater in the elderly, the obese, those with diabetes or other chronic
diseases, patients with sickle-cell disease, Gaucher's disease or
leukaemia, patients on corticosteroid or immunosuppressive
therapy, and patients who have had
multiple previous operations at the same site

mixture of pathogenic bacteria

(Staph, aureus, Proteus, E. coli, Pseudomonas)
Organisms may be introduced directly into the
wound from the atmosphere, the instruments,
The patient or the surgeon
(1)soft-tissue damage
(2)haematoma formation
(3)Bone death

Post Operative Osteomyelitis

'the race for the surface'

(Gristina, 1988)

foreign implant is both a predisposing

factor and an important element in its persistence.
Bacteria as well as human tissue cells have an
affinity for molecules on the surface of the implant.
Both compete for occupancy of the same surface the tissue cells by adaptation and integration, the
bacteria by adhesion and colonization

Early
Intermediate
Late

Post Operative
Osteomyelitis

Post Operative Osteomyelitis

'Prevention is better than cure

(1) avoiding operations on immune-depressed

patients
(2) eliminating any focus of infection before operating
(3) insisting on optimal operative sterility
(4) giving prophylactic antibiotics
(5) handling tissues gently
(6) using high-quality implant materials
(7) ensuring close fit and secure fixation of the
implant
(8) preventing or counteracting later intercurrent
infection

Antobiotics Treatment

Septic arthritis
Septic arthritis; terjadi akibat osteomielitis
pada tulang metaphysis yang terletak intra
capsular
Septic arthritis juga terjadi akibat inokulasi
bakteri langsung ke dalam sendi ,
misalnya trauma tembus ke dalam sendi
atau infeksi menembus jaringan lempeng
epiphysis

Septic arthritis

Septic arthritis
Infeksi bakteri yang menyerang jaringan
synovium dan ruang / kapsul sendi yang
mengakibatkan berkumpulnya reaksi selsel PMN dan ilepaskannya enzym
proteolitik

Infeksi sendi
Septic arthritis
Septic bursitis
Infeksi pada pasien pasca total Hip / knee
replacement

Faktor predisposisi

Peny sendi kronis

Trauma
Rheumatiod arthritis
Diabetes melitus
Terapi steroid
Gagal ginjal
Keganasan
Drug abuse

Riwayat aspirasi
sendi / injeksi
Gangguan /
insufisiensi vascular
Riwayat infeksi sendi
sebelumnya

Sendi predileksi

Lutut 53%
Hip 20%
Bahu 11 %
Siku 17%
Wrist 9 %
Ankle 8 %

Predileksi pada anak :

Paling sering sendi
lutut 39 %
Panggul 32 %

Kuman penyebab

Staphylococcus aureus
Strepticoccus sp
Gram negatif
Pnoumococcus

Kuman penyebab
Anak di bawah 2 th :
Haemophylus influensa

Tes diagnostik
Lab :
Leukosit
LED > 20
Kultur darah
(+)35 %

Pemeriksaan radiologi
Soft tissue : bengkak
Effusi cairan sensi
CT scan
Bone scan Tc 99

Prinsip terapi
Menghambat multiplikasi kuman dg
antibiotik
Drainage abses superiosteal ( bila sudah
terbentuk )

Penatalaksanaan
Kultur resistensi
Antibiotik intra vena : 2- 4 minggu
Operasi drainage

Tuberculosis
(Tuberculosis Osteomyelitis)
Bakteri : Micobacterium Tuberculosa
Humanus droplet infection paru-paru
Bovinus susu usus (jarang)

Pathology
Focus primer komplex primer (lesi paru +
KGB sekitar) bakteri bisa dorman di KGB
bertahun-tahun.

Penyebaran Sekunder
Bila daya tahan tubuh rendah TBC milier di
paru2/meningitis.

Penyebaran Tertier (1)

Penyebaran di luar paru-paru terjadi bertahun-tahun
setelah serangan pertama predileksi di vertebral
body dan sendi synovial besar (panggul dan lutut).
Bakteri bisa dari epiphyse ke synovial atau dari
synovial ke epiphyse atau bersamaan, oleh karena
mendapat nutrisi melalui pembuluh darah yang
sama.

Penyebaran Tertier (2)

Penyebaran tertier terjadi bila daya tahan tubuh
menurun (nutrisi, penyakit kronis).
Bakteri TBC juga bisa menyerang diaphyse
phalanx (tuberculous dactylitis).
Bakteri TBC membentuk granuloma
kumpulan epitheloid dan multi nucleated giant
cell yg mengelilingi jaringan nekrosis, disertai
lymphocyte pada tepinya.

Gejala Klinis
Pembengkakan dan nyeri sendi
terdapat gangguan gerak.
Berat badan menurun.
Night cry.

Spondilitis TBC
Umumnya daerah
thoracolumbal.
Penyebaran melalui
Batsons Plexus dari vena
paravertebral.

 Bakteri umumnya menyerang

bagian anterior vertebral body
osteoporosis dan Sequester
granulasi TBC memenuhi
periosteum Paravertebral
Abses ligamen longitudinal
anterior dan posterior oleh
karena discus intervertebralis
relative kebal, maka kerusakan
terjadi pada stadium akhir hasil
akhir terjadi kyphosis oleh karena
kolaps dari bagian anterior
vertebral body Gibus

Gejala Klinis
Anamnesa
Pembuluh darah : BSE
meningkat, differential
count, PCR TBC.
X-ray
MRI

Therapy
Anti TBC 2 R7H7E7
10 R2H2
Open operation fusi dengan / tanpa
instrumen.

Komplikasi

Potts paraplegia
Oleh karena :
1. Tekanan extra dural
(pus, squester)
2. Penyebaran langsung
ke spinal cord