Pathogenesis

Hematogenous osteomyelitis

Acute hematogenous osteomyelitis is the most common type of bone infection and usually is seen in children. It is more common in males in all age groups affected. Acute hematogenous osteomyelitis is caused by a bacteremia, which is a common occurrence in childhood. The causes of bacteremia are many. Bacteriological seeding of bone generally is associated with other factors such as localized trauma, chronic illness, malnutrition, or an inadequate immune system. In many cases the exact cause of the disease cannot be identified.

When adults are affected, it may be because of compromised host resistance due to debilitation, intravenous drug abuse, infectious root-canaled teeth, or other disease or drugs (e.g., immunosuppressive therapy).

Hematogenous osteomyelitis involves the highly vascular long bones, especially those of the lower limb. Tubular bones have the most rapid growth and the largest metaphyses; therefore, they are common sites of infection. As many as 75% of children have infections in sites such as distal and proximal femur and tibia, distal humerus, and fibula.

In adults, hematogenous spread is more common to the lumbar vertebral bodies than elsewhere.

In children through the age of puberty the long bones of the extremities are most often involved with the metaphysis as the initial infected site (Image 7.1). In adults hematogenous osteomyelitis most often affects the spine. This age-dependent preference for bone relates to the vasculature and blood flow to the site. In children, the metaphysis is very active metabolic tissue with a large blood flow and with vasculature predisposed to infection. Phagocytes lining the capillaries in this region are deficient in number and function. The nutrient arteries near the epiphyseal cartilage are nonanastomosing, thereby allowing any blockage to produce tissue necrosis and the sinusoids (venous side of capillary) have slow, turbulent flow predisposing to thrombosis (Image 7.2). As aging occurs metaphysis metabolism slows down, blood flow decreases and phagocytic activity increases. The metaphysis is commonest site of hematogenous osteomyelitis, because: 1) is highly vascular; 2) has a hair pin like arrangement of capillaries; 3) has sluggish blood flow; 4) has relatively fewer phagocytic cells than the physis or diaphysis, allowing infection to occur more easily in this area; 5) thin cortex.

Image 7.1 Basic anatomy of long tubular bones in children. The most common site of bacterial seeding is the rapidly growing and highly vascular metaphysis of growing long tubular bones.  
Image 7.2 The capillary ends of the nutrient artery are sharp, nonanastomosing loops, which enter the large venous sinusoids. The capillaries do not communicate because columns of calcified cartilage separate them from each other.

Bacterial seeding leads to an inflammatory reaction, which can cause local ischemic necrosis of bone and subsequent abscess formation. As the abscess enlarges, intramedullary pressure increases causing cortical ischemia, which may allow purulent material to escape through the cortex (through Volkmann's canals and the haversian canals) into the subperiosteal space. A subperiosteal abscess then develops.

If left untreated this process eventually results in extensive sequestra formation (sequestrum) and chronic osteomyelitis. The residual dead bone acts as a foreign body, making the eradication of bacteria impossible until the sequestrum is removed.

If the infected area becomes well demarcated and the infection is contained, the acute inflammatory process may subside, leaving a subperiosteal accumulation of pus which may be discovered by tenderness on palpation. This relatively quiescent form of subperiosteal infection is termed a Brodie's abscess. After some time, there is deposition of new bone, the involucrum, under the elevated periosteum.

 

The effects of osteomyelitis in children vary with age based on differences in blood supply and the anatomical structure of the bone (Image 7.3).

¤ In children younger than 2 years, some blood vessels (which is called transphyseal vessels) cross the physis (or epiphysial plate, or growth plate - is a hyaline cartilage plate in the metaphysic at each end of a long bone) and may allow the spread of infection into the epiphysis (Image 7.4).

For this reason, infants are susceptible to limb shortening or angular deformity if the physis or epiphysis is damaged from the infection. The diaphysis rarely is involved, and extensive sequestration occurs infrequently except in the most severe cases.

Image 7.3 Schematic presentation of changing vascular supplies in long bone according to the three different age groups. Basically, the main blood supply to bone ends derives from the nutrient artery. A. In an infant under the age of 18 months small arteries (transphyseal vessels) penetrate the growth cartilage to reach the epiphysis. B. After 18 months, with the involution of the transphyseal vessels, the vascular supply in the epiphysis derives from the epiphyseal arteries and becomes separated from that in the metaphysic by the cartilaginous barrier. C. Following physeal fusion the nutrient arterial branches joined by the epiphyseal branches distribute throughout the whole bone end. The blood supply in the cortex derives from the periosteal artery in the outer zone and from the nutrient artery in the inner zone (by Y.-W. Bahk, 2013).

 

 

Image 7.4 Anatomic considerations that influence the progression of osteomyelitis in children younger than 2 years. The nutrient artery terminates in the metaphysis and sluggishly drains into the venous sinusoids with their slow-moving flow, which results in the formation of metaphyseal osteomyelitis. A. Drawing shows the presence of transphyseal vessels that are patent in the neonate and promote the spread of infection through the relatively avascular physis to the epiphysis, with the infection ultimately decompressing into the joint space. B. Drawing shows an alternate pathway in which the loosely adherent periosteum in the neonate is continuous with the joint capsule, allowing infection to spread directly from the metaphysis to the joint space. (Images by James Federico, 2012)

 

¤ In children older than 2 years of age, the physis effectively acts as a barrier to the spread of a metaphyseal abscess. However, because the metaphyseal cortex in older children is thicker, the diaphysis is at greater risk in these patients. If the infection spreads into the diaphysis, the endosteal blood supply may be jeopardized. With a concurrent subperiosteal abscess, the periosteal blood supply is damaged and can result in extensive sequestration and chronic osteomyelitis if not properly treated (Image 7.5).

 

Image 7.5 The progression of osteomyelitis in the pediatric patient older than 2 years of age (Images by James Federico, 2012).
The nutrient artery terminates in the metaphysis, which drains into the venous sinusoids with their slow-moving flow. Infection develops in this location, with protection of the epiphysis by the relatively avascular growth plate (physis)

 

After the physes are closed, acute hematogenous osteomyelitis is much less common. Hematogenous seeding of bone in adults usually is seen in a compromised host. Although it can occur anywhere and in any part of the bone, generally the vertebral bodies are affected. In these patients, abscesses spread slowly, and large sequestra rarely form. If localized destruction of cortical bone occurs, pathological fracture can result.

In Ukrainian medical school:

There are 4 phases of the development of acute hematogenous osteomyelitis

In children younger than 2 years In children older than 2 years
1 – bone marrow edema 2 – bone marrow abscess / phlegmon 3 – septic arthritis   4 – purulent phlegmon of joint 1 – bone marrow edema 2 – bone marrow abscess (phlegmon) 3 – subperiosteal abscess (phlegmon) 4 – phlegmon of overlying soft tissue