14. Osteomyelitis
What does imaging show of patients with chronic osteomyelitis?
(A) Pain x-ray. In chronic osteomyelitis, a sequestrum may be visible on plain radiographs as a focal calcified mass (dead bone) visible within a radiolucent area (cloaca) completely separated from the surrounding bone. An involucrum can be seen as thick layer of new bone growth outside the segment of the existing bone affected by chronic osteomyelitis. (B) CT scanning. Bone destruction (cloaca), necrotic bone (sequestra), periosteal reaction (involucrum) and sinus tracts are evident on CT. (C) MRI. The sequestrum can be difficult to visualize on MRI. It produces low signal (dark) on all types of images. Cloaca (intraosseous abscess) is visualized as a well-circumscribed area of low signal (dark) on T1-weighted and high signal (bright) on T-2 weighted images. Similarly, draining sinuses and soft tissue inflammation produce a low signal (dark) on T1-weighted images and high signal (bright) on T2-weighted images. The involucrum is hypointense on all types of images and shows gadolinium enhancement.
What is seen on imaging studies of direct contiguous osteomyelitis associated with vascular insufficiency?
(A) Plain x-ray. Bone changes in early osteomyelitis on plain x-rays lag about 2 weeks behind the infection itself. Acute osteomyelitis must extend at least 1 cm and compromise 30-50% of bone mineral content to produce noticeable changes on plain x-rays. Changes may not be obvious until 5-7 days from onset in children and 10 to 14 days in adults. On x-rays taken after this time period, regional osteopenia, focal destructive bony lysis, and periosteal reaction (lifting of the periosteum) may be noted. (B) Computed tomography (CT). CT scanning allows delineation of even the most subtle osseous changes. CT is more sensitive for detection of bony destruction, new bone formation, and periosteal reaction. CT may show these changes earlier than do plain x-ray. CT is unable to demonstrate bone marrow edema, which means that a normal CT cannot diagnose early osteomyelitis. CT does not demonstrate adjacent soft tissue infection. Ct can detect the intramedullary gas, an uncommon but pathognomonic manifestation of osteomyelitis. (C) Magnetic resonance imaging (MRI). MRI is the imaging modality of choice for diagnosing osteomyelitis because of its excellent anatomical detail, high sensitivity for detecting early infection and lack of ionizing radiation. In addition, MRI is able to identify soft-tissue/joint involvement. Bone marrow edema is the earliest feature of acute osteomyelitis seen on MRI and can be detected as early as 1-2 days after the onset of infection. The normal marrow has high T1 signal (bright) due to fat within the medulla. In acute osteomyelitis, the bone marrow becomes congested with fluid and pus, producing low signal (dark) on T1W images and high signal (bright) on T2-weighted images. (D) Technetium radionuclide bone scan (bone scintigraphy). When plain radiographs are normal technetium radionuclide bone scan is the standard screening method for the early evaluation of osteomyelitis. The patient is injected (usually into a vein) with a small amount of radioactive material such as 600 MBq of technetium-99m-methyl diphosphonate (99mTc-MDP) and then scanned with a gamma camera, a device sensitive to the radiation emitted by the injected material. The scan is positive 1-2 days after the onset of infection. The affected site demonstrates increased uptake of the radioisotope.
What are the most common etiologic factors in hematogenous osteomyelitis?
1. Hematogenous osteomyelitis. Hematogenous osteomyelitis is usually monomicrobial. The most common etiologic factors of hematogenous osteomyelitis in children include S. aureus, S. pyogenes and H. influenzae. Children with sickle cell disease have a predisposition to osteomyelitis and there is a tendency for Salmonella organisms to be the infecting agents. It is hypothesized that capillary occlusion secondary to intravascular sickling may devitalize and infarct the gut, permitting Salmonella invasion and bacteremia that can infarct bone. Osteomyelitis is an important complication of drug abuse in adults and the most common causal organisms include Pseudomonas aeruginosa.
What are the three functions of the bone?
1. Supporting function 2. Storage function: mineral storage 3. Metabolic function: the skeleton must maintain the serum level of calcium, phosphate, and magnesium ions.
What are systemic and local complications of osteomyelitis?
1. Systemic complications. Untreated osteomyelitis may lead to systemic infections such as septicemia, bronchopneumonia, and septic pleuritis with life-threatening consequences. 2. Local complications. Local complications are uncommon with current treatment. (A) Pathologic fractures. Pathologic fracture results from a loss of structural integrity of the bone and is a serious complication of osteomyelitis. The extent of osteoporosis surrounding the osteomyelitis area is not appreciated and the child is discharged with the affected limb unprotected. Pathological fractures are slow to heal and may heal in a deformed position. (B) Septic arthritis. Septic arthritis is secondary to discharge of bone purulent exudate into synovial cavity and represents a medical emergency. The inflammatory cells directly destroy the articular cartilage with or without subluxation or dislocation. Often there is no satisfactory reconstruction possible. (C) Growth disturbance. This is due to the destruction of the growth plate or epiphysis and may cause fusion of the epiphysis and diaphysis and premature interruption of longitudinal growth of bone. (D) Squamous cell carcinoma. A long-term risk of long-standing chronic osteomyelitis is malignant transformation (<1% of cases) within a sinus tract and cloaca that have been present for 20-30 years. The most common diagnosis is squamous cell carcinoma arising from the epithelialization of the draining sinus. This complication is also referred to as Marjolin ulcer. This lesion is quite deep within the involved limb, the femur and tibia being the most common sites. This lesion is typically aggressive, and amputation is the most reliable treatment. (E) Amyloidosis. Amyloidosis is characterized by the extracellular deposition of an abnormal fibrillar protein (AA protein) in tissues. Amyloidosis is diagnosed by rectal biopsy. Patients have a mean duration of chronic osteomyelitis of 4.5 years.
In adults, where does acute hematogenous occur? What are the most common sources of infection? What would labs show?
Acute hematogenous osteomyelitis in the adult is relatively rare. Most cases are observed in patients over age 50. It is usually seen in vertebrae, with involvement of the intervertebral disc (called 'discitis') which is generally considered the primary source of the infection. Disc expands with pus and bores into adjacent vertebrae, most commonly lumbar (60%) followed by thoracic spine (30%) and cervical spine (10%); occasionally is manifested as spinal epidural or paraspinal abscess. The most common sources of bacteremia seeding vertebral bodies are urinary tract infections, infective endocarditis, and intravenous drug use. The most common pathogens are S. aureus, followed by E. coli and Pseudomonas. The clinical onset is usually insidious with symptoms of back pain and sometimes fever (40%). Laboratory findings include leukocytosis, elevated ESR and CRP. Blood cultures are positive in 50% of cases. Complications include vertebral collapse and spinal cord compression with neurologic compromise (weakness or sensory loss).
How is osteomyelitis treated?
Antimicrobial therapy for osteomyelitis often is initiated before the diagnosis is confirmed. Agent selection is done empirically taking into consideration the age of the patient and any special features. Treatment may be modified once the organism is identified. If clinical improvement with reduction in fever and local signs of inflammation fails to occur over 24-48 hours, the most likely cause is formation of an abscess which requires surgical drainage, resection of necrotic bone, and debridement of fistula.
What is chronic osteomyelitis?
By definition, acute osteomyelitis becomes "chronic" after duration of 1 month. Acute osteomyelitis and chronic osteomyelitis are therefore considered to be the same disease at different stages. Patients with chronic osteomyelitis have a history of acute hematogenous and direct contiguous osteomyelitis not treated correctly.
What is the pathology of chronic osteomyelitis?
Chronic osteomyelitis is a long-standing suppurative bone infection that often evolves over months or even years. Chronic osteomyelitis is characterized by persistence of bacteria with low- grade suppurative inflammation, sequestrum and fistulous tracts. Morphologically there are necrotic bone fragments (sequestrum) surrounded by dense fibrotic tissue infiltrated by mononuclear cells surrounding a persistent, pus-producing central cavity (cloaca). Chronically draining sinus tracts through the skin to the surface of the body are a common feature of chronic osteomyelitis. A shell of reactive bone (involucrum) forms around the affected segment of the bone (long bone metaphysis or diaphysis).
How does direct contiguous osteomyelitis present clinically?
Clinical manifestations include localized pain, erythema, swelling and drainage from wound infection. Fever and systemic features are conspicuously absent. Any bone can be involved. The tibia is the most frequent site of post-traumatic osteomyelitis. Spread from decubitis ulcer may involve the sacrum, trochanter and heels.
What is the most common etiology of direct contiguous osteomyelitis associated with vascular insufficiency?
Diabetic foot osteomyelitis is also polymicrobial with S. aureus predominating, but Gram negative bacteria like Proteus, E. coli and anaerobes Peptococci and Bacteroides are often present.
How does direct contiguous osteomyelitis occur? Which bacteria are likely responsible?
Direct contiguous osteomyelitis is seen most often in three circumstances: (i) after trauma, such as open wounds or fractures; (ii) none surgery with placement of metallic orthopedic implants, and (iii) pread from adjacent extraskeletal focus such as infected sinuses, infected teeth, decubitus ulcer, and puncture wounds of feet. Contiguous osteomyelitis is a polymicrobial infection. S. aureus is the most common pathogen; S. pyogenes, enterococci, Clostridium spp, and Bacillus spp. are also frequently isolated.
What is the most common etiologic factor for direct contiguous osteomyelitis?
Direct contiguous osteomyelitis is usually polymicrobial. The most common etiologic factors include S. aureus, E. coli, and Pseudomonas species. S. aureus is still preponderant, but it is usually associated with other organisms including anaerobes (Bacteroides species). Osteomyelitis complicating open fractures is most commonly due to hospital-acquired pathogens such as S. aureus. Osteomyelitis complicating soil contaminated wounds is often due to Clostridium perfringens. Osteomyelitis complicating direct trauma in immunocompromised hosts is often due to Candida, Cryptococcus and Aspergillus species. Orthopedic metal implants are known to promote S. aureus-induced osteomyelitis thanks to the S. aureus ability to form biofilms in the metallic surfaces. Pseudomonas aeruginosa is commonly isolated in osteomyelitis following puncture wounds of foot. Osteomyelitis complicating cat and dog bites is most often due to Pasteurella multocida. 3. Direct contiguous osteomyelitis associated with vascular insufficiency. Diabetic foot osteomyelitis is also polymicrobial with S. aureus predominating, but Gram negative bacteria like Proteus, E. coli and anaerobes Peptococci and Bacteroides are often present.
Which group is most commonly affected by direct contiguous osteomyelitis?
Direct contiguous osteomyelitis secondary to open fracture affects males in the 2nd or 3rd decade of life. While the incidence of acute hematogenous osteomyelitis has decreased, bone infections by direct inoculation have increased. This is due to high-energy accidents and the growing use of orthopedic fixation devices and joint prostheses.
What is the sequestrum, involucrum, and cloaca?
Fragments of necrotic bone can separate within the abscess cavity to form a sequestrum (Latin: 'to set apart'). The sequestered dead bone fragments are usually removed by osteoclasts when small; larger fragments may require surgical removal. As pus lifts the periosteum there is new bone proliferation in order to wall off the infectious process. This thick bony collar is often referred to as an involucrum (Latin: 'to wrap'). The thick bone sleeve usually envelops the affected segment of the shaft; and in cases of extensive lesions, almost the entire shaft may become encased in involucrum. The occurrence of a defect that may develop in the involucrum is referred to as a cloaca (Latin: 'sewer'). The function of cloaca is to allow continued discharge of inflammatory products from the bone into soft tissues. If the draining tract extends to the skin surface, the portion extending beyond the involucrum to the skin surface is called a sinus tract. Cutaneous fistula drains pus and bacteria to the skin surface. Cloaca, draining sinus tracts and fistulae are most frequently associated with chronic osteomyelitis, which is stubborn in its response to conventional antibiotic therapy.
What would labs show in a patient with acute hematogenous osteomyelitis?
Laboratory findings demonstrate leukocytosis, elevated C-reactive protein (CRP) level and erythrocyte sedimentation rate (ESR). Blood cultures are positive in half of cases.
How does chronic osteomyelitis present clinically?
Long-standing bone pain, continuous drainage of pus through the skin via a sinus tract, an area of skin erythema around the affected bone, swelling and tenderness, no fever or low-grade fever and general malaise are some of the most commonly reported clinical symptoms.
What is the pathology of acute osteomyelitis?
Morphologically, acute osteomyelitis is characterized by a purulent inflammatory exudate composed of numerous neutrophils, fibrin, and macrophages. The inflammation is located primarily in the medullary spaces of the cancellous bone. Marrow spaces are filled with neutrophils, necrotic debris, and microorganisms. Marrow fatty tissue and hematopoietic marrow undergo necrosis and are replaced by inflammatory exudate. Pressure in the medullary space is increased and blood vessels are destroyed. As a result, compromised vascular perfusion leads to additional necrosis of cancellous and compact bone. Osteocytes die and osteocyte lacunae appear empty. Sequester formation may ensue.
Who is affected by osteomyelitis? (age/sex)
Osteomyelitis is a relatively uncommon condition. Its incidence is 2 cases in 100,000 individuals per year. Osteomyelitis demonstrates a biphasic age distribution. The first peak occurs in children younger than 14 years (hematogenous osteomyelitis). The second peak occurs in persons older than 50 years of age (contiguous osteomyelitis and osteomyelitis of the diabetic foot). There is a 2:1 male-to-female ratio with a higher frequency in boys attributed to levels of activity and associated minor trauma. In the preantibiotic era, the mortality rate was as high as 25-40%. Antibiotics have reduced associated mortality to almost 0%.
How is direct contiguous osteomyelitis associated with vascular insufficiency diagnosed? Bacteriologically and through biopsy?
Osteomyelitis is known as the "great pretender", due to difficulties of diagnosis. Several conditions can present similar symptoms. Often patients lack fever, erythema and drainage. The correct diagnosis is usually based on blood culture, bone biopsy, plain film radiography and radionuclide bone scan (bone scintigraphy). 1. Bacteriological diagnosis. Blood cultures yield growth only in 50% of cases of hematogenous osteomyelitis. In direct contiguous osteomyelitis secondary to local trauma, blood cultures are mostly negative. Cultures of subperiostal pus obtained through needle aspiration are positive in 75% of cases. 2. Biopsy diagnosis. Specimens of imaging-guided core bone biopsies or material curetted at surgery show fragments of mineralized necrotic bone debris (no living osteocytes within lacunae) surrounded by numerous acute inflammatory cells (neutrophils). The blood vessels are congested. This is the classic histopathologic presentation of acute osteomyelitis.
What is osteomyelitis?
Osteomyelitis is the progressive infection of bone and bone marrow by microorganisms resulting in inflammatory destruction of bone, bone necrosis, and new bone formation.
What is the clinical presentation of acute hematogenous osteomyelitis?
Patients usually present within several days to one week after the onset of symptoms. Typical clinical findings include pain, erythema, swelling, and warmth over the involved bone and decreased range of motion in adjacent joints. In addition to local signs of inflammation and infection, patients have signs of systemic illness, including fever, irritability and lethargy.
How does acute osteomyelitis spread in the bone towards the epiphysis? Specifically describe how it does this in infants, children, and adults.
Spread of infection toward the epiphysis. Hematogenous osteomyelitis begins with implantation of the offending organism in the medullary tissues. Purulent inflammation develops at the level of the cartilaginous growth plate. Bone necrosis is an important feature of osteomyelitis. The inflammatory edema within a rigid bone tissue results in mechanical compression of the capillaries leading to infarction of bone. A purulent exudate forms (abscess) surrounding the dead bone and spreads in planes of least resistance. Pathways of infection spread differ in the infant, child, and adult. These differences are inherent to patterns of blood supply to the epiphysis of long bones. INFANTILE PATTERN. In infants, metaphyseal blood vessels may penetrate the cartilaginous growth plate and supply the epiphysis. These vessels allow the spread of the infection toward epiphysis with consequences such as destruction of epiphysis and spread of inflammation into the joint space. Infectious arthritis, or pyarthrosis, is a common complication in infantile osteomyelitis CHILDHOOD PATTERN. The vascular barrier at the growth plate becomes complete by the end of the first year of life. After this time, no metaphyseal blood vessels penetrate the growth plate and the epiphyseal blood supply is distinct and separate. The blood flow through metaphysis is slow and turbulent causing bacteria to be trapped in the metaphysis. For these reasons, hematogenous osteomyelitis in children has a predilection for metaphysis and spares the epiphysis. ADULT PATTERN. In the adult, the metaphyseal vessels gradually penetrate the vanishing cartilaginous growth plate, re-establishing communication between the metaphysis and the epiphysis (subarticular end of the bone). This explains the increased incidence of septic arthritis secondary to osteomyelitis in adult patients.
What is subacute osteomyelitis?
Subacute osteomyelitis, also termed Brodie abscess, is a chronic low-grade infection of bone characterized by a lack of systemic manifestations. This form of osteomyelitis was initially described by the British surgeon Sir Benjamin Collins Brodie in 1832. The clinical manifestations of osteomyelitis depend on the interplay between the pathogen and the host. Subacute osteomyelitis represents a favorable host-pathogen response, i.e., a good host resistance with a low virulence of the infective organism. If acute osteomyelitis is characterized by septic clinical course, subacute osteomyelitis presents a low-grade clinical course. Subacute osteomyelitis generally occurs in patients <25 years of age. It is usually of hematogenous origin. The disease has an insidious onset and mild symptoms. Pain is the most common symptom and has usually been present for several months before the initial evaluation. Swelling and tenderness over the area of involved bone may also be seen. Laboratory evaluation is unrevealing. There is no leukocytosis; the erythrocyte sedimentation rate (ESR) may also be normal. Pathological findings include an intramedullary abscess located the metaphysis of long bones of the leg. The abscess cavity is usually round, measuring 1-4 cm in diameter. This cavity is filled with pus lined by granulation tissue and surrounded by thick sclerotic bone. There is no sequestrum. The culture of the pus is positive in 50% of cases and S. aureus is the most common pathogen. Plain x-ray shows a well-defined round or ovoid radiolucency with thick surrounding sclerosis.
Who is affected by chronic osteomyelitis?
The large majority of patients are between 21 and 60 years of age. The median age at diagnosis is 45 years.
How does acute osteomyelitis spread towards the periosteum?
The medullary abscess expands, and osteoclastic activity resorbs the existing bone. New, reactive, woven bone is formed but fails to wall off the infection. Eventually, the pus discharges within Volkmann canals to subsequently form a subperiosteal abscess with periostitis and lifting of the periosteum. This process occurs readily in infants because they have few Sharpey's fibers and the periosteum is easily stripped from the bone. Lifting of the periosteum causes loss of blood supply to the cortical bone, rendering it necrotic. Note that periosteal arteries constitute a vascular plexus lying on the outer surface of the periosteum, which anastomoses with adjacent skeletal muscles. Periosteal arteries supply the outer one-third of cortex.
What is the most common etiologic factor of osteomyelitis?
The most common etiologic factor is Staphylococcus aureus (80-90% of cases). The normal bone is highly resistant to infection, but S. aureus possess a variety of virulence factors. S. aureus cells express surface proteins that promote attachment to host proteins such as laminin and fibronectin of the extracellular matrix. With these receptors, the bacteria binds to surfaces in the extracellular matrix, and also to plates, screws, polymers used in orthopedic surgery, forming complex colonies known as biofilms. Biofilm shields the bacteria from the outside environment. The biofilm-like properties make the infections tenacious and tough. In many cases, physicians are left with surgical debridement as the only option to remove the invading bacteria and achieve a sterile site.
What is the primary site of infection for acute hematogenous osteomyelitis in children?
The most common sites of involvement are the long bones (femur, tibia, and humerus). Infection starts in the metaphyseal region near the epiphyseal growth plate of long bones. The metaphyseal vessels are terminal branches of the nutrient artery, which penetrates the diaphyseal cortex through the nutrient foramen located approximately at mid-shaft. The terminal branches of metaphyseal vessels make a hairpin bend, retreating back upon themselves and flow into a large network of sinusoidal veins. At those hairpin bends, the rate of blood flow is greatly reduced. This is thought to account for the localization of blood-borne bacteria that causes the onset of hematogenous osteomyelitis.
What bacteria cause chronic osteomyelitis?
The most commonly involved pathogen is by far Staphylococcus aureus. Methicillin-resistant S. aureus (MRSA) has also been increasingly isolated from chronic osteomyelitis lesions. Other causative pathogens include Staphylococcus epidermidis, Pseudomonas aeruginosa, Serratia marcescens and Escherichia coli. Mycobacterial and fungal infections are generally uncommon and are often associated with immunodeficiency.
What is direct contiguous osteomyelitis associated with vascular insufficiency?
This type of osteomyelitis accounts for 30% of cases and occurs in people with type 2 diabetes mellitus. The major factor predisposing diabetic patients to osteomyelitis has traditionally been considered to be diminished blood supply. Recent observations suggest that diabetic neuropathy is a more important factor. Osteomyelitis follows a neuropathic foot ulcer developing over a prominent bone until seeding of the underlying bone occurs. Diabetics can be particularly susceptible to a challenging form of osteomyelitis. Infections originate from a diabetic foot ulcer. Diabetic foot ulcers are open sores that occur most often on the heel, plantar metatarsal head areas, and the tips of the toes. The pathophysiologic mechanisms of diabetic ulceration include atherosclerosis of limb arteries, diabetic neuropathy, pressure from poorly fitted shoes, and foot deformity. Infected diabetic foot ulcer shows local signs of inflammation (erythema and warmth) and purulent discharge. Bone pain is often absent by the associated neuropathy. A laboratory findings indicating osteomyelitis is ESR of more than 70 mm/hr. The infection is polymicrobial but S. aureus predominates. Delay in diagnosis increases amputation risk! MRI is the most sensitive imaging study to identify bone infection; plain x-ray changes develop late. Bone biopsy through unaffected skin is the gold standard of diagnosis.
What is hematogenous osteomyelitis?
This type of osteomyelitis accounts for 20% of cases and occurs during a bacteremic event and results in seeding of the bone. In children, metaphysis of the long bones is most often involved; in adults, lumbar vertebral bodies are most often involved. The infection is monomicrobial, and S .aureus is preponderant
What is direct contiguous osteomyelitis?
This type of osteomyelitis accounts for 50% of all cases. The bone is seeded from adjacent infections of the surrounding soft tissues. These infections can result from penetrating trauma, or an operative wound, such as bone surgery, or joint replacement. It can occur at any age and can involve any bone. It tends to involve multiple organisms (S. aureus is preponderant). This type of osteomyelitis is due to spread from a contiguous focus of infection. It is caused by bacteria which gain access to bone by direct inoculation.
