Hematogenous osteomyelitis

In 1831 Raynaud introduced the term "osteomyelitis" which means inflammation of the bone marrow Nowadays the word "osteomyelitis" denotes a suppurative process affecting all components of bone

Purulent osteomyelitis can be of two types

a. b.

hematogenous osteomyelitis traumatic osteomyelitis

gunshot osteomyelitis postoperative osteomyelitis

Hematogenous osteomyelitis
patients

with hematogenous osteomyelitis comprise 3-10% children and teenagers (7-15 years old ) boys suffering about three times more often than girls hematogenous osteomyelitis becomes chronic and lasts for many years

Etiology
Hematogenous osteomyelitis is characterised by monoinfecton Staphylococcus aureus Streptococci Pneumococci Colibacilli

Pathogenesis
a

small purulent focus (a suppurating scratch, a boil or abscess in lymphoid follicle ) or a consequence of serious purulent processes bacteriemia purulent focus of the bone - osteomyelitis

Pathogenesis

a.

peculiarities of structure of a child's bone in the area of its growth

metaphysis has a large vascular network with wide capillaries with slow flow Metaphyseal vascular network is not connected with apiphyseal vascular network metaphyseal vessels (arterioles) have a dead end In children's spongy bone there are vulnerable trabecules

b.
c.

d.

Pathogenesis

Microorganisms die in the bone marrow being destroyed by macrophages. Microorganisms cause a purulent process immediately. Microorganisms remain as a latent infection without clinical manifestations which can cause the process upon weakening of the body's resistance sometimes several years after penetration.

Pathogenesis
Sometimes trauma of the bone can be the factor weakening local resistance to infection while pyogenic agents invaded the bone earlier, perhaps by hematogenous route. In almost half of all cases the attack of acute hematogenous osteomyelitis is preceded by a trauma. Children's infections, flu, cooling are factors reducing the general resistance of the body.

Pathologoanatomical presentations
necrotisation of

nearby trabecules and vascular

thrombosis processes spread in the direction of diaphysis bone marrow necrotises and gets dissolved by pus - abscess of bone marrow pus spreads under the periosteum through haversian spaces - subperiosteal abscess intermuscular phlegmon fistula

Clinical presentations
general symptoms The disease is often preceded a local purulent process or injury of the extremity deterioration of general condition sudden rise of temperature to 39C profuse vomiting, delirium sepsis for several days

Clinical presentations
local symptoms
It is especially difficult to reveal local symptoms in the first days of disease. Complaint: local painfulness in the corresponding bone, amplifying upon axial load

there is no swelling or redness in this area Only in 7-10 days: local symptoms of intermuscular phlegmon (swelling and redness) Afterwards pus can come outside forming a fistula

Diagnosis

leucocytosis, deviation of the differential blood count to the left X-ray findings in the first two weeks of disease are negative Afterwards: picture of periostitis Still later, areas of rarefaction in metaphysic appear

2-4 months after the onset of the disease: formation of sequesters (separate areas of necrotized bone tissue)

Diagnosis
fistulography
tomography

thermography
isotope

and ultrasound investigation radiothermy

General treatment

Antibiotic therapy
semisynthetic penicillines, lincomycine, cephalosporines

Aggressive detoxication therapy

crystalloid solutions, blood substitutes with a detoxicating effect and blood plasma, laser and ultraviolet irradiation of blood, hemosorption

Immunocorrection and symptomatic therapy

Local treatment

plaster bar surgical treatment

dissection of soft tissues dissection of intermuscular phlegmon creation of trephine openings through the bone placement of drains

treatment
In the postoperative period the treatment is administered according to general principles of treating suppurative wounds; immobilisation is obligatory until a complete control of inflammation.

Chronic hematogenous osteomyelitis

Chronic hematogenous osteomyelitis is a disease where there is typically a purulent-necrotic focus in the bone and a fistula. This condition is of long duration and cannot heal by itself.

Etiopathogenesis
Chronic

osteomyelitis is always preceded by an acute stage The transition into a chronic form can take place in 3 weeks to 4 months from the onset of disease The sequestration process proceeds very slowly taking months and sometimes years

Clinical presentations
the clinical course is characterised by few signs

gnawing pains the area of osteomyelitic focus purulent fistulas postoperative scars When the process exacerbates, the pains become sharp, the temperature rises to 38-39C, the skin in the area of osteomyelitic fistula becomes hyperemic

Diagnosis

a. b. c. d. e. f.

X-ray signs of chronic osteomyelitis

thickening of the bone cavities sequesters osteosclerosis narrowing of medullary canal thickening of periosteum Fistulography, tomography, scintillography and especially computer tomography

Treatment
Antibiotic

therapy Detoxication therapy Immunocorrection therapy Surgical treatment

Surgical treatment

removing the sequesters reparative surgery of bone cavity

a. b. c.

d.

plasty with pedicle flap from surrounding muscles bone grafting using vascularised tissue flaps metals with memory

Atypical forms of chronic osteomyelitis

Brodie's

abscess Sclerosing osteitis (Garre's disease) Albuminous osteomyelitis

Brodie's abscess
Limited necrosis of spongy bone (mostly in the proximal part of tibial bone) develops forming an abscess which can be detected by X-ray. Treatment includes trephination of the cavity and draining (musculoplasty is seldom used, only in large abscess).

Garre's disease
Osteomyelitis is characterised by subacute uneventful course, phlegmons and fistulas do not develop, sclerotic change of affected bone prevails which can be detected by Xray. Against the background of sclerosis foci of bone destruction are noted. The treatment is usually conservative, only if necrotic foci are large, surgical intervention is indicated.

Albuminous osteomyelitis
Pathogenesis of this disease is not quite clear. No purulent exudate forms in the focus of inflammation but serous fluid rich in albumines is accumulated. General symptoms are moderately pronounced. Sequestration of bone tissue develops seldom and slowly. Exacerbation of the process can be associated with secondary purulent infection. Surgical treatment like in chronic hematogenous osteomyelitis is indicated.

Complications of chronic osteomyelitis

deformity of

tubular bones articular ankylosis pathological fractures, false joints, ununited fractures, bone defects malignant transformation of the walls of osteomyelitic fistulas amyloidosis of inner organs