Osteomyelitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2],Nate Michalak, B.A.

Osteomyelitis is an infection of bone or bone marrow, usually caused by pyogenic bacteria or mycobacteria. It can be subclassified on the basis of the causative organism, the route, duration and anatomic location of the infection.^[1]

Osteomyelitis has been described since antiquity and evidence of the disease exists in dinosaur fossils. The disease used to be called “abscessus in medulla”, “necrosis” and “boil of the bone marrow” until Auguste Nelation coined the term osteomyelitis in 1844. NJ Blockey, JT Watson, and TA McAllister developed treatment strategies for osteomyelitis in 1970 upon which current clinical practices are based.

Entry of the organism into bone is the first step in the development of osteomyelitis and it occurs via three main mechanisms:^[2][3]

• Hematogenous seeding
• Contiguous spread of infection to bone from adjacent soft tissue
• Direct inoculation from trauma or orthopedic surgery (including prostheses).

Microbial and host factors contributing to the pathologic process of the disease may vary from one patient to another. In children, the long bones are usually affected. Acute osteomyelitis almost invariably occurs in children. In adults, the vertebrae and the pelvis are most commonly affected, possibly due to the compromised host resistance as a result of debilitation, intravenous substance abuse, infectious root-canaled teeth, or other disease or drugs (e.g., immunosuppressive therapy).

Common causes include: Staphylococcus aureus, Streptococcus pyogenes, Haemophilus influenzae, Enterobacter, Escherichia coli, Pseudomonas, Streptococcus pneumoniae, Mycobacterium tuberculosis.

Two classification schemes are currently used. Lew and Waldvogel classified osteomyelitis according to the duration and mechanism of infection into hematogenouos osteomyelitis, contiguous-focus osteomyelitis, and osteomyeltis secondary to vascular insufficiency. Cierny and Mader classified osteomyelitis according to the anatomy of bone infection and host physiology. This systems classifies the location of infection into 4 stages and the host’s physiology into 3 levels of compromise.

Osteomyeltis must be differentiated from other diseases that cause ostealgia, edema, and erythema, including soft tissue infection (commonly cellulitis or erysipelas), Charcot arthropathy, osteonecrosis, gout, fracture, bursitis, and malignancy.

Incidence of osteomyelitis is approximately 13 per 100,000 in children and approximately 90 per 100,000 in adults. Hematogenous osteomyelitis occurs predominantly in children and elderly patients while osteomyelitis due to contiguous infection is most common in adults. Osteomyelitis is more common in males but there is no racial predilection. The disease is more common in developing countries.

Risk factors for osteomyelitis include diabetes, hemodialysis, immunosuppression, tuberculosis infection, injection drug use, poor blood circulation, sickle-cell disease, recent trauma, and orthopedic surgery.

Symptoms begin several days to weeks after infection. Symptoms lasting approximately less than 14 days is considered acute osteomyelitis, while longer lasting symptoms constitute chronic osteomyelitis. Acute symptoms include a prodrome accompanied by local erythema, edema, warmth, and pain. Patients with chronic osteomyelitis develop sinus tracts or sequestra. Bearing weight may become increasingly difficult and patients may develop soft tissue ulcers, nonhealing fractures, and Brodie’s abscess. Complications include bone destruction, amputation, contiguous infection of joints or soft tissue, impaired bone growth in children, or neoplasm. Prognosis is generally good for acute osteomyelitis but usually poor for patients with chronic osteomyelitis.

The patient’s history is important to establish a diagnosis of osteomyelitis. Common findings in the history include intravenous drug use, bacteremia, recent open fracture or surgery, and diabetes. Common symptoms include chills, fever, malaise, local pain and warmth, edema, and erythema. Fever is typically absent in diabetic patients with osteomyelitis secondary to vascular insufficiency and patients with an infected prosthesis.

Patients with acute osteomyelitis may present with fever, local swelling, redness, and tenderness. Patients with chronic osteomyelitis may present with additional signs such as bone sequestra, draining sinus tracts, thickened periosteum, unhealing ulcers, unhealing fractures, Brodie’s abscess, and unstable joints in cases of infected prosthesis. Commonly affected bones include the long bones and lumbar vertebrae in hematogenous osteomyelitis, hips, knees and elbows in contiguous-focus osteomyelitis, and foot bones in osteomyelitis secondary to vascular insufficiency.

Diagnosis of osteomyelitis is often based on radiologic results showing a lytic center with a ring of sclerosis, though bone cultures are normally required to identify the specific pathogen. Conventional radiographic evaluation of acute osteomyelitis is insufficient because bone changes are not evident for 14–21 days after the onset of infection.

Although MR imaging is the accepted modality of choice for the early detection and surgical localization of osteomyelitis, CT scan is usually more readily available for establishing the diagnosis in the emergency department.^[4]

On a CT scan, features of bacterial osteomyelitis include overlying soft-tissue swelling, periosteal reaction, medullary low-attenuation areas or trabecular coarsening, and focal cortical erosions.

MR imaging is the accepted modality of choice for the early detection and surgical localization of osteomyelitis.

Osteomyelitis often requires prolonged antibiotic therapy, with a course lasting a matter of weeks or months. A central catheter (PICC line) or central venous catheter is often placed for this purpose. Initial first line antibiotic of choice is determined by the patient’s history and regional differences in common infective organisms. Prior to the widespread availability and use of antibiotics, blow fly larvae were sometimes deliberately introduced to the wounds to feed on the infected material, effectively scouring them clean.^[5][6] Hyperbaric oxygen therapy has been shown to be a useful adjunct to the treatment of refractory osteomyelitis.^[7][8] A treatment lasting 42 days is practiced in a number of facilities.^[9]

Osteomyelitis may also require surgical debridement. Severe cases may lead to the loss of a limb.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nate Michalak, B.A.

Osteomyelitis has been described since antiquity and evidence of the disease exists in dinosaur fossils. The disease used to be called “abscessus in medulla”, “necrosis” and “boil of the bone marrow” until Auguste Nelation coined the term osteomyelitis in 1844. NJ Blockey, JT Watson, and TA McAllister developed treatment strategies for osteomyelitis in 1970 upon which current clinical practices are based.

• Osteomyelitis has been identified in the fractured spine of a dimetrodon Permian reptile, which existed 291 to 250 million years ago.
• Osteomyelitis may have been been first described by Hippocrates (460-370 BC).
• Before Auguste Nelation termed the disease “osteomyelitis” in 1844, the disease was referred to as “abscessus in medulla”, “necrosis”, and “boil of the bone marrow”.
• Prior to the introduction of penicillin in 1940 as an antibiotic, osteomyelitis was usually treated with crude surgical excision of necrotic tissue or limb amputation.
• Penicillin significantly reduced mortality until 1950 following the emergence of penicillin-resistant bacteria, most commonly Staphylococcus spp
• In 1970, NJ Blockey, JT Watson, and TA McAllister reevaluated the treatment of osteomyelitis with antibiotics and surgery, which reflects current clinical practices.^[1]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nate Michalak, B.A., Seyedmahdi Pahlavani, M.D. [2]

There are many classification systems for osteomyelitis. In general, there are three major classification systems which include; classification according to the symptom chronology, Lew and Waldvogel classification, and Cierny and Mader classification. Osteomyelitis may be classified according to the symptom chronology into acute, sub-acute (further subdivided into the Glendhill and Robert et al. systems), and chronic. Chronic osteomyelitis may be subdivided into Lew and Waldvogel’s classification system and Cierny and Mader’s classification system. Osteomyelitis may be classified according to Lew and Waldvogel’s system based on the duration and mechanism of infection into 3 subtypes which are; hematogenouos osteomyelitis, contiguous-focus osteomyelitis, and osteomyeltis secondary to vascular insufficiency. Osteomyelitis may be classified according to Cierny and Mader’s classification system based on the anatomy of bone infection (4 stages) and host physiology (3 levels of compromise).

There are many classification systems for osteomyelitis:

• Osteomyelitis may be classified according to symptom chronology into acute, sub-acute (further subdivided into the Glendhill and Robert et al. systems), and chronic
• Lew and Waldvogel classified osteomyelitis according to the duration and mechanism of infection (traditional classification)^[1]
• Cierny and Mader classified osteomyelitis according to the anatomy of bone infection and host physiology^[2]

• The Cierny and Mader system offers a guide to treatment

• Acute osteomyelitis: Osteomyelitis is classified as acute if the duration of the disease has been less than 2 weeks.
• Sub-acute: Sub-acute hematogenous osteomyelitis has a more insidious onset and lacks the severity of symptoms, which makes the diagnosis of this disorder difficult. Typically, diagnosis is delayed for more than 2 weeks.

• Chronic Ostemyelitis: Chronic osteomyelitis is defined as persistent pain, erythema, or swelling, sometimes in association with a draining sinus tract that mostly lasts for more than 4 weeks.
  

The following table describes the classification schemes for chronic osteomyelitis.

Lew and Waldvogel Etiologic System

Cierny and Mader Staging System

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Entry of the organism into bone is the first step in the development of osteomyelitis and occurs by three main mechanisms; hematogenous seeding, contiguous spread of infection to bone from adjacent soft tissue, and direct inoculation from trauma or orthopedic surgery (including prostheses).^[1][2]

Microbial and host factors contributing to the pathological process of the disease may vary from one patient to another. In children, the long bones are usually affected. Acute osteomyelitis almost invariably occurs in children. In adults, the vertebrae and the pelvis are most commonly affected, possibly due to the compromised host resistance as a result of debilitation, intravenous substance abuse, infectious root-canaled teeth, or other disease or drugs (e.g., immunosuppressive therapy).

Entry of the organism into bone is the first step in osteomyelitis and occurs by three main mechanisms:^[1][2]

1. Hematogenous seeding
2. Contiguous spread of infection to bone from adjacent soft tissue
3. Direct inoculation from trauma or orthopedic surgery (including prostheses).

Several factors contributing to the pathogenesis of osteomyelitis include microbial factors and host factors.

• Etiologic pathogen possesses numerous cell-wall associated adhesins mediating specific attachment to a wide variety of extracellular matrix proteins found in bone including, fibronectin, laminin, osteopontin, bone matrix sialoprotein, and collagen.^[2]
• After attachment to the bone matrix, direct toxin effect of pathogen may lead to tissue necrosis.
• Adherent bacterial growth leads to the formation of a biofilm (an adherent consortium of micro-organisms enmeshed in an exocellular polysaccharide).^[3]
• Biofilm pathogens are more resistant to host defense and are able to survive longer than usual.^[3]

Host factors that may contribute to the pathogenesis of osteomyelitis are subdivided into factors that are involved in hematogenous spread and factors that may contribute to contiguous spread.

• The pathogen colonizes the metaphysis of a large long bone below the growth plate.
• In adults, after closure of the growth plate, the metaphyseal and epiphyseal vessels establish reconnections so bacteria entering the nutrient artery are directed to the vascular loops beneath the articular cartilage.
• Accordingly, acute hematogenous osteomyelitis in infants and adults often affects the epiphysis.
• In children the growth plate acts as an barrier and the infection is limited to the metaphysis.^[4]
• Extension across the growth plate is impeded in children but after closure of growth palate, joint involvement becomes possible.
• In the spine, blood-borne pathogens usually localize to the subchondral regions of the vertebral body.

• In contiguous spread, bone adjacent to a cutaneous or mucosal ulcer or soft tissue abscess are affected.
• It is more commonly observed in the setting of periodontal and sinus disease, cellulitis of diabetic feet, epidural abscess, decubitus ulcer, or septic arthritis.^[5][6]
• In this setting, the inflammatory process must first destroy the periosteum or articular surface before it accesses the bone.
• Unlike hematogenous osteomyelitis, the cortex instead of the medullary cavity is initially infected, and the site at which this occurs influences the rapidity of spread and extent of disease.

• Pathogens trigger inflammation and due to this inflammatory process, intraosseous pressure inside the tight bone matrix increases and may lead to thrombosis of bone vasculature that finally results in bone death.
• If the infection progresses, pus may track to other areas of the bone along the medullary canal or through the Haversian systems in cortical bone from the medulla to the outer surface of the cortex and form a subperiosteal abscess.
• This may contribute to bacteremia or it may track out into the soft tissues and eventually form abscesses or a sinus tract draining to the outside.
• Dead bone accelerates biofilm formation.
• Both the inflammatory cytokines and mediators released during infection, and in some cases bacterial products themselves, can trigger bone resorption either by osteoclast activation or by stimulating phagocytic cells to take on a bone-resorbing phenotype.^[7]
• Bone loss starts around the dead area, resulting in the separation of the dead area of bone from the surrounding living bone, ultimately, forming theSequestrum.
• When periosteal stripping occurs, the resulting periosteal reaction produces a shell of new bone; the Involucrum, around the dead bone.

• Factors that may commonly complicate osteomyelitis are fractures of the bone, amyloidosis, endocarditis, or sepsis.

• Osteomyelitis is a secondary complication in 1-3% of patients with pulmonary tuberculosis. In this case, the bacteria generally spread to the bone through the circulatory system, first infecting the synovium (due to its higher oxygen concentration) before spreading to the adjacent bone. In tubercular osteomyelitis, the long bones and vertebrae are the ones often affected.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

The etiology of osteomyelitis include a wide range of microbes, organized based on prevalence in patients of different age groups.

Etiolgic agents of osteomyelitis can be classified in several ways.

• Staphylococcus aureus

• Streptococcus pyogenes

• Haemophilus influenzae

• Enterobacter

• Escherichia coli

• Pseudomonas

• Streptococcus pneumoniae

• Mycobacterium tuberculosis

• Cellulitis

• Septic arthritis

• Fracture

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Osteomyeltis must be differentiated from other diseases that cause ostealgia, edema, and erythema, including soft tissue infection (commonly cellulitis), Charcot joint, osteonecrosis, gout, fracture, bursitis, and malignancy.

Osteomyeltis must be differentiated from other diseases that cause bone pain, edema, and erythema. The following table summarizes the differential diagnosis for osteomyelitis.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nate Michalak, B.A.,Seyedmahdi Pahlavani, M.D. [2]

Incidence of osteomyelitis is approximately 13 per 100,000 in children and approximately 90 per 100,000 in adults. Hematogenous osteomyelitis occurs predominantly in children and elderly patients while osteomyelitis due to contiguous infection is most common in adults. Osteomyelitis is more common in males but equally affects each race. The disease is more common in developing countries.

• The annual incidence of pediatric osteomyelitis is approximately 13 per 100,000 individuals.^[1]
• The annual incidence in adult osteomyelitis is approximately 90 per 100,000 individuals.^[2]

• Osteomyelitis occurs in all patient age groups.

• Hematogenous osteomyelitis occurs predominantly in children and elderly patients.
• The most common form of the disease in adults is osteomyelitis due to contiguous infection, resulting from trauma or surgery.
• Vertebral osteomyelitis typically occurs in patients older than 50 years of age.

• Osteomyelitis occurs more commonly in males for unknown reasons.^[3][2]

• Osteomyelitis occurs equally among all races.^[4]

• Osteomyelitis is more common in developing countries.^[5]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2], Nate Michalak, B.A.

Risk factors for osteomyelitis include diabetes, hemodialysis, immunocompromised patients, tuberculosis infection, IV drug use, poor blood circulation, sickle-cell disease, recent trauma, and orthopedic surgery.

Risk factors associated with osteomyelitis could be divided to 2 major categories; systemic factors and local factors:^[1][2][3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nate Michalak, B.A., Seyedmahdi Pahlavani, M.D. [2]

Symptoms begin several days to weeks after infection. Symptoms lasting approximately less than 14 days is considered acute osteomyelitis, while longer lasting symptoms constitute chronic osteomyelitis. Acute symptoms include a prodrome accompanied by local erythema, edema, warmth, and pain.

Patients with chronic osteomyelitis develop sinus tracts or sequestra. Bearing weight may become increasingly difficult and patients may develop soft tissue ulcers, nonhealing fractures, and Brodie’s abscess. Complications include bone destruction, amputation, contiguous infection of joints or soft tissue, impaired bone growth in children, neoplasm, or tumor. Prognosis is generally good for acute osteomyelitis but usually poor for patients with chronic osteomyelitis.

• Acute infection is typically defined as symptoms lasting less than 14 days and if left untreated it may lead to chronic osteomyelitis.^[1]

• Patients typically develop prodromal symptoms after several days such as fever, malaise, irritability, lethargy, and chills.
• Local symptoms soon follow the prodrome and include erythema, edema, warmth, and pain.

• Chronic osteomyelitis is defined as the presence or recurrence of symptoms for greater than 4 weeks.

• Patients with chronic osteomyelitis may develop sequestra.
• Patients may continue presenting with acute symptoms and bearing weight may become increasingly difficult.
• Patients may develop soft tissue ulcers, nonhealing fractures, and Brodie’s abscess.^[2]

The following complications can occur:^[3][4]

• Sepsis
• Bone destruction
• Pathologic fractures
• Limb amputation
• Depending on the location of osteomyelitis, local extension of an invasive, suppurative process can lead to septic arthritis, brain abscess, meningitis, spinal cord compression, pneumonia, and empyema.
• Impaired bone growth in children
• Sinus tract formation may be associated with neoplasms, especially in the setting of longstanding infection.^[5][6][7]

• Most common: squamous cell carcinoma
• Less common: fibrosarcoma, myeloma, lymphoma, plasmacytoma, angiosarcoma, rhabdomyosarcoma, and malignant fibrous histiocytoma

• With treatment, the outcome for acute osteomyelitis is usually good.^[8]
• Prognosis is usually poor for patients with chronic osteomyelitis, even with surgery.

• Amputation may be needed, especially in those with diabetes or poor blood circulation.
• Patients with chronic osteomyelitis may have recurring symptoms after treatment.

• The outlook for those with an infection of an orthopedic prosthesis depends on:

• The patient’s immunity status
• The type of infection
• Whether the infected prosthesis can be safely removed