Osteomyelitis literally means inflammation of bone and its marrow regardless of whether it is due to pyogenic organisms, tuberculosis, syphilis, a specific virus, or the presence of a foreign.
However, its more accepted meaning is the infection by pyogenic bacteria or less commonly to the other organisms. The infection involves the marrow spaces, the Haversian canals, and the subperiosteal space.
Bone is normally resistant to bacterial colonization but trauma, surgery, foreign bodies, or the placement of prostheses may disrupt bony integrity and cause bone infection.
Osteomyelitis can be acute or chronic. An acute osteomyelitis occurring on pre-existing chronic osteomyelitis is termed as acute on chronic osteomyelitis.
Approximately 20% of adult cases of osteomyelitis are hematogenous. Osteomyelitis are more common in males for reasons not known.
In children, the long bones are usually affected. In adults, the vertebrae and the pelvis are most commonly affected.
Post traumatic osteomyelitis [47%], vascular insufficiency [as in diabetics] [34%] and hematogenous seeding [19%] are major causes of osteomyelitis.
Post traumatic group of osteomyelitis includes injuries and use of orthopedic hardware to manage trauma.
In children acute hematogenous osteomyelitis secondary to nidus of infection is the major cause of osteomyelitis.
The most common organisms isolated in these cases include S aureus, Streptococcus pneumoniae, and Haemophilus influenza type b which has become less common since the use of vaccine for H influenza type b. Pseudomonas species or Escherichia coli are common causes of infection after puncture wounds of the feet or open injuries.
Osteomyelitis in neonates also results from hematogenous spread, especially in patients with indwelling central venous catheters. Here the most common organism involved is group B Streptococcus species, and E coli.
Children with sickle-cell disease are susceptible to bacterial infections and the most common organisms involved in osteomyelitis is Salmonella species followed by S aureus, Serratia species, and Proteus mirabilis.
Following table shows age wise common different infecting organisms.
|Age group||Most common organisms|
|Newborns [< 4 months]||S. aureus, Enterobacter species, and group A and B Streptococcus species|
|Children [4 months to 4years]||S. aureus, group A Streptococcus species, Haemophilus influenzae, and Enterobacter species|
|Children, adolescents (4yeras to adult]||S. aureus (80%), group A Streptococcus species, H. influenzae, and Enterobacter species|
|Adult||S. aureus and occasionally Enterobacter or Streptococcus species|
|Sickle cell anemia patients||Salmonella species are most common in patients with sickle cell disease.|
Most of the patients affected with vertebral osteomyelitis are older than 50 years. The infection usually originates hematogenously. Vertebral osteomyelitis generally involves two adjacent vertebrae with the corresponding intervertebral disc. The lumbar spine is most commonly affected, followed by the thoracic and cervical regions.
Pathophysiology of Osteomyelitis
Factors important in the pathogenesis of osteomyelitis include
- Virulence of the infecting organism
- Underlying disease,
- Immune status of the host
- Location and vascularity of the bone.
- Bacterial Properties
- Bacterial adherence
- Resistance to host defense mechanism
- Proteolytic activity
In adults, the vertebrae are the most common site of hematogenous osteomyelitis, but infection may also occur in the long bones, pelvis, and clavicle.
Primary hematogenous osteomyelitis is more common in infants and children, usually occurring in the long bone metaphysis. Secondary hematogenous osteomyelitis occurs when a childhood infection is reactivated.
In adults also, the location of hematogenous osteomyelitis is metaphyseal. Potential sources of infection include skin, soft tissue, respiratory tract, genitourinary tract, infected intravenous sites, and dental infections
In hematogenous osteomyelitis S aureus, pseudomonas and enterobacteriae are main affecting organisms. Gram negative organisms are less common but could occur in gastrointestinal or genitourinary infections. Pseudomonas aeruginosa is more common in intravenous drug users.
During bacteremia, an infective embolus enters the nutrient artery and is trapped in a small vessel. Most of the small end-arteries and capillaries are located in the metaphysic adjacent to the epiphyseal plate which explains the predilection of the metaphysic to infection.
Infective embolus blocks a small vessel, and a small area of bone become necrotic. Hyperemia develops and brings inflammatory factors.
The hyperemia results in decalcification of the surrounding bone.
The inflammatory factors and leukocytes destroy bacteria, necrotic bone, and medullary elements. The debris and the exudates increase in amount and effect pressure within the rigid unyielding walls of bone. Other blood vessels are compressed, and further bone necrosis ensues. The exudates follows paths of least resistance, mainly through the Haversian and the cortical Volkmann canals to enter the subperiosteal space.
Here, an accumulation of exudates gradually strips the periosteum as a subperiosteal abscess. The periosteum to wall off the infection by forming new trabeculae of bone. The underlying cortex, deprived of its periosteal blood supply, becomes necrotic. Perforation of the periosteum permits spread of the infection in the soft tissues.
The exudates may spread down the medullary canal, destroying marrow elements and the blood supply to the cancellous bone and inner aspect of the cortex.
In an advanced stage, the cortex may be surrounded externally and internally by pus and deprived of its blood supply resulting in sequestration of entire diaphysis.
Therefore early decompression is important.
Epiphyseal plate forms a great barrier to infection. Therefore the spread to adjacent joint is rare.
To spread to joint, the pus must penetrate the periosteum, spread along the soft tissues, and penetrate the capsule. The hip is an exception as the metaphysic there is intracapsular and direct spread can occur.
Healing may occur in natural course or under the influence of antibiotics.
An intervention in very early stage [antibiotic therapy] may be able to cure the infection before bony destruction has started.
When minimal destruction of the bone has occurred, the exudates is resorbed, and new bony trabeculae are formed. Organisms of lesser virulence and inadequate resistance may result in the formation of a persisting abscess surrounded by a fibrous membrane and walled off by a ring of dense bone.
This is known as Brodie’s abscess.
The infection may be reactivated at any time, or the organisms are destroyed and a cavity containing sterile pus, serous fluid, or fibrous tissue will remain indefinitely.
When the dead bone is large, it is gradually separated from living bone [sequestrum] and is slowly destroyed. Because it has no blood supply, the sequestrum appears to be dense in comparison with surrounding decalcified bone.
Sequestrum persists until it is slowly resorbed or extruded. Until this happens, exudates is formed continually and may drain externally. Walled-off areas of infection may undergo recrudescence of activity at any time in later years. This is the stage of chronic osteomyelitis.
Contiguous-focus and Post Traumatic Osteomyelitis
Infection introduced through an external wound usually causes a chronic osteomyelitis.
The infection may occur due to
- Direct inoculation of bacteria via trauma,
- During surgical reduction and internal fixation of fractures
- Insertion of prosthetic devices
- From local soft-tissue infection
- From adjacent septic arthritis
- Nosocomial contamination.
In this type of spread, the infection usually results approximately one month after inoculation.
Tibia is most common bone affected and adults are more commonly affected.
The most commonly isolated organism is S aureus.
An hematogenous infection spreads from inside out whereas, post traumatic infection begins outside the bony cortex and works its way in toward the medullary canal.
Low-grade fever, drainage, and pain may be present. Loss of bone stability, necrosis, and soft
Septic arthritis is more common in neonates than in older children and is often associated with metaphyseal osteomyelitis.
Patients with diabetes have vascular compromise and are at greater risk of developing osteomyelitis when soft tissue infection or ulcer is present as in foot.
Patients with vascular compromise, as in diabetes mellitus, are predisposed to osteomyelitis owing to an inadequate local tissue response and even minor trauma can result in osteomyelitis. Sreptococcus species, Enterococcus species, coagulase-positive and negative staphylococci, gram-negative bacilli, and anaerobic organisms are most commonly isolated.
When the original acute bone infection has subsided, it may persist as a low-grade infection subject to repeated recrudescences of the acute process over many months or years. Hematogenous infection with an organism of low virulence may be chronic from the onset. Traumatic osteomyelitis is chronic from onset.
We have discussed the sequestrum formation. Separation of dead bone from living may require several months.
After complete sequestration, so that the dead fragment lies free within a cavity, the surrounding living bone attempts to wall off the infection by forming a thick, dense wall, the involucrum.
When neighboring tissue is destroyed, the surface of the sequestrum remains uneroded. Externally, the periosteum lays down new bone to form an involucrum.
Rarely, the entire shaft will sequestrate and be enveloped by a new periosteal bone casing that gradually increases in density and thickness.
An involucrum usually has multiple openings, the cloacae, through which exudates, bone debris, and sequestra find exit and pass through sinus tracts to the surface. Constant destruction of neighboring soft tissues leads to cicatrix formation.
Thinning of skin and inward growth of the skin in the skin is thin, distorted, and easily traumatized, the skin epithelium growing inward to line the sinus tracts.
After a sequestrum has been discharged or removed, the sinus usually closes, and the cavity may fill with new bone especially in children.
In adults, the cavity may persist and harbor organisms that may reactivate the infection at any time.
In chronic osteomyelitis of long standing, multiple cavities and sequestra exist throughout the bone. The shaft becomes thickened, irregular, and deformed.
Staging of Osteomyelitis [Cierny-Mader]
This staging system considers host immunocompetence in addition to anatomic bony involvement and histologic features of osteomyelitis.
Involves medullary bone and is usually caused by a single organism
Involves the surfaces of bones and may occur with deep soft-tissue wounds or ulcers
- Advanced local infection of bone and soft tissue
- Polymicrobial [multiple types of organisms], often due to infected intramedullary rod or open fracture
- Responds well to limited surgical intervention that preserves bony stability
- Extensive disease involving multiple bony and soft tissue layers
- Complex disease that requires a combination of medical and surgical therapies
- Requires post-surgical stabilization as an essential part of therapy
Physiologic status of the host
Normal physiologic, metabolic, and immune functions
Systemic (Bs) or local (Bl) immunocompromise or both (Bls)
Treatment poses a greater risk of harm than osteomyelitis itself
The state of the host is the strongest predictor of osteomyelitis treatment failure, and thus the physiologic class of the infected individual is often more important than the anatomic stage
Clinical Presentation of Osteomyelitis
A history of antecedent infection may or may not be available.
With the onset of osteomyelitis, symptoms of a severely acute illness appear. The child is irritable and restless.
Headache, high-grade fever with chills occur.
The affected limb is held in semiflexion, surrounding muscles are in spasm due to excruciating pain.
On examination, there is tachycardia and patient resists the passive movement of the affected limb due to muscle spasm.
The affected site is tender to deep palpation.
Initially, swelling is not present but within a few days the soft tissues about the affected site become edematous and red, indicating subperiosteal abscess formation.
Tenderness is quite pronounced.
Fluctuation may be elicited if the pus has escaped outside the periosteum.
Sometimes, sympathetic effusion may be seen in the neighboring joint.
In children, the clinical presentation of osteomyelitis can be challenging because it can present with only nonspecific signs and symptoms
Newborns with osteomyelitis may demonstrate decreased movement of a limb without any other signs or symptoms.
A previous history of acute ostemyelitis may be available. In case of traumatic osteomyelitis, the nature and mode of injury is asked.
In post surgical cases, the details of surgery and follow-up should be available.
Patient may complain of local pain, swelling, erythema, and edema may also be reported.
On physical examination, scars or local disturbance of wound healing may be noted .
During the period of inactivity, no symptoms are present.
In long-standing cases, the is thickens and the skin is dusky, thin, scarred, and poorly nourished. Muscles are scarred and cause contractures of adjacent joints. A lighting up of infection is manifest by aching pain that is worse at night.
As the infection progresses, a sinus may open and drain indefinitely, extruding small sequestra at intervals. Spontaneous closure of the sinus and subsidence of infection often occur.
These recurrent acute flare-ups occur at indefinite intervals over months and years. A sinus may drain continuously.
- Acute Rheumatic Fever
- Ewing’s Tumor
- Acute Suppurative Arthritis
A complete blood count is useful for evaluating leukocytosis and anemia. Leukocytosis is common in acute but is usually normal in chronic osteomyelitis. Erythrocyte sedimentation rate and C-reactive protein levels are usually increased.
Blood cultures are positive in only 50% of cases of osteomyelitis.
Aspiration of subperiosteal pus reveals by culture the infecting organism and its sensitivity to antibiotics.
Bone biopsy leads to a definitive diagnosis by isolation of pathogens directly from the bone lesion but the procedure is not required in all the cases.
Acute osteomyelitis presents with acute inflammatory cells, edema, vascular congestion, and small-vessel thrombosis, necrotic bone shows extensive resorption and inflammatory exudates, including polymorphonuclear leukocytes, macrophages, and osteoclasts.
A sequestrum is formed when dead cortical bone is gradually detached from living bone.
Chronic osteomyelitis presents with pathologic findings of necrotic bone, formation of new bone, and polymorphonuclear leukocyte exudation, a large numbers of lymphocytes, histiocytes, and occasional plasma cells.
Films are negative within the first week or 10 days.[ These changes may take until 5-7 days in children and 10-14 days in adults to appear on x-ray]. Serial x-rays may help monitor development of the lesion.
Thereafter, a localized area of bone destruction is observed in the metaphysic surrounded by a wide zone of decalcified bone. Later, within the next few weeks, the periosteal shadow is elevated at the same level, and multiple laminations of bone deposition parallel with the shaft are seen.
Further destruction gives an appearance of a moth eaten pattern of destruction
Sequestrum appears denser than the surrounding decalcified bone. When healing takes place in the earliest stage, the bony architecture is quickly restored.
Radiographic findings include periosteal thickening or elevation, as well as cortical thickening, sclerosis, and irregularity.
Plain films show lytic changes after at least 50%-75% of the bone matrix is destroyed. Therefore, negative radiographic studies do not exclude the diagnosis of acute osteomyelitis.
Healing fractures, cancers, and benign tumors may appear similarly on plain film. Subtle changes may indicate contiguous-focus or chronic osteomyelitis.
In chronic osteomyelitis, in the early stages, the bone appears moth-eaten and osteoporotic, and areas of sclerosis develop. The periosteum is elevated by subperiosteal laminations of new bone, which become progressively thicker and dense.
Sequestrum becomes surrounded by a white ring representing reactive new bone formation, the involucrum. A sequestrum may not be visible because of overlying dense bone.
X-ray exposures with varying intensities and from various projections may be needed.
Compted tomography defines the bony lesions better and is also useful for guiding needle biopsies in closed infections . It helps to assess bony integrity, cortical disruption, and soft-tissue involvement.
Edema, itraosseous fistula and cortical defects can be demonstrated on CT.
Magnetic Resonance Imaging
MRI is able to detect osteomyelitis in very early stages and helps to gauge the success of the treatment.
It shows extent and location of osteomyelitis along with pathologic changes of bone marrow and soft tissue.
Ultrasound can demonstrate fluid collection adjacent to the bone, elevation and thickening of the periosteum.
Nuclear Medicine Imaging
Three-phase bone scanning is helpful in evaluating acute osteomyelitis and doubtful lesions.
For this study , white blood cells labeled with technetium-99m (99mTc) hexamethylpropylene amine oxime (99mTc-HMPAO) or indium-111 (111In) oxime are used.
The specificity is less in cases of secondary osteomyelitis.
Positron Emission Tomography
2-[18F]fluoro-2-deoxy-D-glucose (18F-FDG) positron emission tomography may provide high-resolution tomographic images in spinal lesion.
Treatment of Osteomyelitis
An antibiotic is started even before diagnosis can be established definitely.
Cephalosporins are preferred antibiotics. Antibiotics must cover gram negative bacteriae also. As the infection is in closed space, immediate decompression by evacuation of pus should be done at the earliest possible opportunity, even before signs of subperiosteal infection are evident.
Standard treatment of the acute osteomyelitis is surgical [exploration and evacuation].
But if the offending organism and appropriate antibiotic can be determined from blood culture within a reasonable period, vigorous antibiotic treatment without surgical drainage may be sufficient to effect a cure. Surgery is indicated if the patient does not respond to treatment.
Conservative treatment is not to be considered if there is soft tissue abscess or subperiosteal collection, or if concomitant joint infection.
Antibiotics for Osteomyelitis Treatment
The choice of antibiotic agent is based on the identification of pathogens from bone cultures at the time of bone biopsy or debridement.
Parenteral [intravenous] and oral antibiotics may be used alone or in combination .
Antibiotic therapy generally consists of 4- to 6-week course.
Oral antibiotics that have been proven to be effective include clindamycin, rifampin, trimethoprim-sulfamethoxazole, and fluoroquinolones.
Linezolid is active against methicillin-resistant staphylococci and vancomycin-resistant Enterococcus.
Oral quinolones are often used in adults for gram-negative organisms.
Rifampicin must always be used in combination with other antibiotics for prosthesis infections. Rifampicin acts on the biofilm and avoids recurrence.
Staging of the osteomyelitis guides the treatment.
Stage 1 and 2 disease usually do not require surgical treatment, whereas stage 3 and 4 respond well to surgical treatment. In class C hosts, treatment may be more harmful than the osteomyelitis itself.
Operative treatment consists of
- Adequate drainage
- Debridement of necrotic tissue
- Dead space obliteration
- Adequate soft-tissue coverage
- Restoration of blood supply.
- External fixation when a fracture is
No treatment is necessary when asymptomatic.
Antibiotics are given in acute exacerbations.
- Removal of hardware if present
- Removal of sequetrum if present
- Saucerization of the bone to debride bone cavities
- Repeat debridement may be necessary
- Bone grafting and soft tissue coverage procedures
- Closed irrigation and suction
- Local antibiotic coated beads
Complications of Osteomyelitis
The most common complication in children with osteomyelitis is recurrence of bone infection. Impaired bone growth especially when the growth plate is affected.
Inadequate therapy may lead to relapsing infection and progression to chronic infection though chronic infection may still develop in 5-10% of patients treated appropriately.
Because of the avascularity of bone, chronic osteomyelitis is curable only with radical resection and in extreme cases, amputation.
Ssecondary amyloidosis, and squamous cell carcinoma at the sinus tract cutaneous orifice are rare complications.
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