Osteomyelitis overview
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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],Nate Michalak, B.A.
Overview
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]
Historical Perspective
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.
Pathophysiology
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).
Causes
Common causes include: Staphylococcus aureus, Streptococcus pyogenes, Haemophilus influenzae, Enterobacter, Escherichia coli, Pseudomonas, Streptococcus pneumoniae, Mycobacterium tuberculosis.
Classification
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.
Differentiating Osteomyelitis from Other Diseases
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.
Epidemiology and Demographics
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
Risk factors for osteomyelitis include diabetes, hemodialysis, immunosuppression, tuberculosis infection, injection drug use, poor blood circulation, sickle-cell disease, recent trauma, and orthopedic surgery.
Natural History, Complications, and Prognosis
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.
Diagnosis
History and Symptoms
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.
Physical Examination
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.
Laboratory Findings
X Ray
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.
CT
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.
MRI
MR imaging is the accepted modality of choice for the early detection and surgical localization of osteomyelitis.
Treatment
Medical Therapy
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]
Surgery
Osteomyelitis may also require surgical debridement. Severe cases may lead to the loss of a limb.
Presentation on Osteomyelitis
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References
- ↑ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 810-811 ISBN 978-1-4160-2973-1
- ↑ Gristina AG, Oga M, Webb LX, Hobgood CD (1985). "Adherent bacterial colonization in the pathogenesis of osteomyelitis". Science. 228 (4702): 990–3. PMID 4001933.
- ↑ Clarke SR, Foster SJ (2006). "Surface adhesins of Staphylococcus aureus". Adv. Microb. Physiol. 51: 187–224. doi:10.1016/S0065-2911(06)51004-5. PMID 17010697.
- ↑ Laura M. Fayad, John A. Carrino, and Elliot K. Fishman. Musculoskeletal Infection: Role of CT in the Emergency Department. RadioGraphics 2007 27: 1723-1736.
- ↑ Baer M.D., William S. (1931). "The Treatment of Chronic Osteomyelitis with the Maggot (Larva of the Blow Fly)". Journal of Bone and Joint Surgery. 13: 438–475. Retrieved 2007-11-12.
- ↑ McKeever, Duncan Clark (2008). "The classic: maggots in treatment of osteomyelitis: a simple inexpensive method. 1933". Clin. Orthop. Relat. Res. 466 (6): 1329–35. doi:10.1007/s11999-008-0240-5. PMID 18404291. Unknown parameter
|quotes=ignored (help); Unknown parameter|month=ignored (help) - ↑ Mader JT, Adams KR, Sutton TE (1987). "Infectious diseases: pathophysiology and mechanisms of hyperbaric oxygen". J. Hyperbaric Med. 2 (3): 133–140. Retrieved 2008-05-16.
- ↑ Kawashima M, Tamura H, Nagayoshi I, Takao K, Yoshida K, Yamaguchi T (2004). "Hyperbaric oxygen therapy in orthopedic conditions". Undersea Hyperb Med. 31 (1): 155–62. PMID 15233171. Retrieved 2008-05-16.
- ↑ Putland M.D, Michael S., Hyperbaric Medicine, Capital Regional Medical Center, Tallahassee, Florida, personal inquiry June 2008.