23.07.

2010

Pathogenesis of the acute hematogenous osteomyelitis

Infection spreads from the primary endogenous focus via the blood
leading to embolism of the feeding the bone vessel. That form
commonly affects young teenage boys.

Bone osteomyelitis Pathogenesis of the acute posttraumatic osteomyelitis

Osteomyelitis represents nonspecific purulent-necrotic process with Posttraumatic osteomyelitis is caused by secondary contamination of
alteration of bone (osteitis), bone marrow (myelitis), periosteum compound bone fractures, gunshot wounds, and as a complication of
(periostitis), and surrounding tissues. The term was introduced by orthopedic surgery
Reynauld at a1831

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Classification of osteomyelitis
Hematogenous (endogenous).
Pathogenesis of the hematogenous and posttraumatic osteomyelitis
Postraumatic (exogenous).

Classification of osteomyelitis according to course of

Etiology of osteomyelitis
disease and clinical picture

Form of
Responsible microbes Toxic form
osteomyelitis
Staphylococcus
Associations
Anaerobes Septicopyemic form
(G+ and G -)
Local form

Hematogenous 60-85% 8-10% 3-5%

Posttraumatic 60-70% 60-70% 10-20%

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Clinical manifestation of acute hematogenous osteomyelitis

First days of infection: general signs of infection are marked. Change Laboratory diagnosis
of general condition, signs of intoxication. Local status: scarce data
(localized pain over metaphysis, special maneuvers)
Laboratory changes are not specific.
Bl d culture
Blood l h
has to b
be obtained
b i d (b(before
f
antibacterial treatment if possible)
At early stage an intraosseal pressure may be
measured

Instrumental diagnosis
Local picture of osteomyelitis of the ribs and breastbone in several
Characteristic radiologic picture becomes obvious only 12-14 days
days after onset of symptoms. Local clinical picture becomes more
after beginning of the disease (thickening of the periosteum, vague
evident.
contour of the bone morrow channel)

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Treatment
Within first 48 hours the pus has not yet been loculated and an
infection may be aborted by appropriate AB, splintage, and parallel
infusion and detoxication therapy. After that period the pus must be
evacuated through a wide incision.

Continuous irrigation of a former

osteomyelitic area is done after surgery

Intensive medical therapy is necessary to patients with acute

hematogenous osteomyelitis or severe traumatic damages when a
Forms of primary chronic osteomyelitis are the following
patient develops pronounced clinical picture of inflammation with
endotoxicosis, or even sepsis syndrome.
Antibacterial therapy Brodie’s abscess
R l i h
Replenishment off circulating
i l i volume
l d iimprovement off
and G
Garre’s
’ di
disease
peripheral circulation
Ollier’s albuminous osteomyelitis
Detoxication therapy
Correction of anemia and hypoproteinemia
Intermittent local pain, absence of sequesters and fistula are the
Correction of fluid-electolyte and acid-base disorders
commonest signs for all the primary-chronic forms. Usually they
Immunotherapy (if indicated) result from py
pyogenic
g septicemia
p from which the patient
p has
Enteral (parenteral) nutrition recovered, leaving the bone abscess which may remain dormant
Local wound treatment (use of controlled abacterial for years (due to low virulent bacteria, good host defense, exposure
environment, local care according to stage of wound to antibiotics)
healing)

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Garre’s sclerosing osteomyelitis is characterized by osteitis of the

Brodie’s abscess affects diaphysis of the tibia, usually as a single
diaphysis and induration of bone tissue with periosteum leading to
bone cavity.
widening of the bone.

Ollier’s albuminous osteomyelitis commonly affects brachium or

femoral bone, usually as a multiple bone cavities filled with serous
Reasons of chronic osteomyelitis
fluid.

Natural outcome of nontreated acute osteomyelitis

I d
Inadequate surgical
i l treatment off acute
osteomyelitis
Inadequate antibacterial treatment of acute
osteomyelitis

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Chronic osteomyelitis may result from any form of acute

osteomyelitis. It is accompanied by necrosis of segment of the bone
(sequester), suppuration, and purulent fistula formation. Sometime it Laboratory and instrumental investigation
is complicated by pathologic fracture.
Usual analyses
Microscopy of the wound swab
Bacteriologic exam (culture, sensitivity)
X-ray (plane and special: tomo-, sinography)
CT
MRI
R di
Radionuclide
lid examination
i ti
Dopplerography of soft tissue vessels
Angiography (if indicated)

Suppuration and purulent fistula are the distinctive features of local

manifestation of the chronic osteomyelitis. The course of disease is CT is useful to estimate extend and character of bone destruction,
characterized by wave-like alternation of relapse of symptoms and position of the sequestra at the bone channel
remission that may last for several weeks to years.

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CT is also able to evaluate condition of paraossal soft tissues Radionuclide investigation (scintigraphy) may roughly estimate the
(paraossal phlegmon is visible on СT) size of osteomyelitic focus

Fistulograpy (or sinography) provides precise information about

CT picture of breastbone osteomyelitis localization, size of the bone cavity, and extension of the pus at the
soft tissues

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Basic principles of surgical treatment After radical resection of necrotized part of the bone the left gap at
the bone and soft tissues must be closed. Different methods of
Radical surgical debridement of primary suppurative focus, excision of closure are given below
all nonviable tissues and necrotized parts of the bone
Replacement of bone defect:
Surgical debridement is accompanied by physical methods of antisepsis
(pressurized
( i d pulsatile
l il iirrigation
i i off the
h wound d using
i antiseptics,
i i Vascularized tissue flap
ultrasound, and laser). Illisarov’s technique
Free distant bone or tissue flap
Adequate active continuous draining of the wound and bone cavity
using special plastic perforated drains after surgery.
Replacement of soft tissue defect:
Local tissues (direct approximation)
Bone plasty is followed by sufficient stabilization of bone fragments
using external fixation apparatus. Method of ggradual tissue extension
Skin graft
Replacement of the defect of soft tissues using different types of plastic Tissue flap (local, migrating, or free flap)
methods. Combination of aforementioned techniques
Cateterization of the ipsilateral main artery and intraarterial
administration of antibiotics of diseased extremitymay be done

Surgical treatment
Surgical intervention may require resection of affected bone part
(necrsequesterectomy). Resection of part of the bone is indicated if
more than half of bone circumference is involved into the pathologic
process, or if a false joint has formed.
Small defects may be closed using modern implants based on the
collagen, antibiotics and other organic substances. A bone defect can
be closed by a muscle flap.

Exposure of the bone Resection of part of the bone

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If the segment of the bone has been destroyed by osteomyelitis the Primary closure by direct wound edges approximation
Illisarov’s technique (external fixation device) is convenient After treatment of bone focus the wound may be covered using local
tissues if they are not changed above the bone

An extensive bone defect may require the use of an osseous flap Method of gradual tissue extension can be used if complete wound
shaped from the fibula (bone segment with surrounding tissues) closure is impossible to achieve after surgery. The sutures are
gradually tied.

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If the local tissues are limited the distant migrating pedicled flap
(Italian plasty, cross-leg flap) may be transferred from the another
Skin graft is useful to cover extensive defects of the skin
area of the body

Local tissue flap is used to create the tissue «bulk» above the Free tissue flap may be used but it requires special microvascular
affected bone technique, skillfulness, and possesses high number of complications

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Suppurative arthritis
is a purulent inflammation of the joint. It represents nonspecific
purulent necrotic process in the joint and paraarticular tissues.
Suppurative arthritis must be differentiated with other more common
non-purulent inflammations of joints which are possible at patients
with Raitre syndrome, rheumatic arthritis , systemic lupus
erytematosis,
i etc.))
Classification:
1. Exogenous: open joint damage (posttraumatic), injections
(postinjection), after orthopedic surgery (postoperative)
2. Endogenous is caused by septic embolus traveled from
distant areas where the primary infection focus is located.
23.07.2010
Patophysiologic stages of development of endogenous arthritis
1. Serous arthritis represents inflammation in the synovial bursa and
accompanied by collection of effusion in the joint.
2. Contamination of effusion results in joint empyema.
3. Further progress of infection onto the joint surfaces, joint’s
caps le and ligaments leads to panarthritis
capsule,
4. If an inflammation extends onto the bone epypheses and
methaphyses the condition is named osteoarthritis.
Diagnosis
Patient complaints: pain at the affected joint. General signs of
infection
History of present complaints
Examination of a local status: local signs of infection, effusion
(ballottement of «floating patella», bulge sign), etc.
Laboratory picture is not specific
Instrumental facilities: joint plane X-ray, CT, MRY, ultrasound
Bacteriologic examination
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Intensive medical therapy is indicated to patients with severe
infection, pronounced clinical picture of inflammation with
endotoxicosis
Antibacterial therapy
Surgical treatment
1st and 2nd stage of disease (without joint destruction): puncture and
draining of the joint. Draining with active continuous irrigation using
antiseptics is preferred. Antibacterial drugs are administered
systemically

R l i h
Replenishment off circulating
i l i volume
l and
d iimprovement
of peripheral circulation
Detoxication therapy
Correction of anemia and hypoproteinemia
Correction of fluid-electolyte and acid-base disorders
Immunotherapy (if indicated)
Immobilization of affected joint at the position of
function

Draining is necessary when it is still possible to save anatomo-

functional integrity of the joint. Continuous irrigation lasts for 20-25
days.

Aspiration of fluid from

different joints

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3rd stage of disease (with destruction of joint) requires arthrotomy,

excision of all necrotic tissues, and resection of affected joint
surfaces. Surgery is finished by continuous active draining of the
joint. Irrigation is continued till all the signs of arthritis will have
disappeared. Joint immobilization and arthrodesis is accomplished
using external fixation device.

Wide arthrotomy and Resection of bone ends

excision of all necrotic tissues

4th stage of disease (osteoarthritis) needs another approach.

Plastic tube placement Closure of the defect

(for postoperative active irrigation) by different types of plasty

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If a bone defect is less than 3 cm the compressive arthrodesis using

external fixation device is convenient.
If a bone defect exceeds 3 cm firstly the compressive arthrodesis is
performed. When the length of the extremity is restored using
Illisarov’s technique of distraction ostheosynthesis accomplished
using external fixation device.

Arthrodesis invariably leads to loss of joint function.

The former joint is stiff, but weight-bearing function of extremity is saved.

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