Osteomyelitis

 

Pathogenesis

Microflora in Osteomyelitis

Staphylococcus Aureus remains the most common pathogen, but the percentage of, hematogenous osteomyelitis

due to S. aureus has declined from 80 % to 90 % of cases to 40% to 605 in recent years .

Staphylococcus Epidermidis causes approximately 5% or fewer cases of disease. Because inadvertent contamination of cultures by the organism is frequent, its role as a pathogen in unknown. Group A Streptococci isolates cause disease in children and occasionally in adults.

Group B Streptococci.  

Are common in neonates and may be more common pathogen in this age group than are Staphylococci. Group B Streptococci also occur in diabetic patients .
Haemophilus Influenza is now an infrequent cause of osteomyelitis in the United States due to widespread usage of polysaccharide vaccine Gram negative enteric bacilli mostly Escherichia coli, Salmonella and Klebsiellaspecies, most
often occur in adults and account for 10% to15% of cases of hematogenous osteomyelitis. Gram negative infections are common in certain predisposed hematogenous osteomyelitis e.g. Neonates (Enterobacteriacae),patients with sickle cell disease (Salmonella),and intravenous drug users(Pseudomonas).Patients with underlying chronic illness, including chronic renal disease, alcoholism,diabetes, andmalignancy, also have an increased risk of gram- negativeinfections. Anaerobes are uncommon cause of hematogenous osteomyelitis. Infections with multiple organisms (multiple infections) are not uncommon [6].

Mycobacterium Tuberculosis

 Tuberculous osteomyelitis should be suspected in any of vertebral osteomyelitis or osteomyelitis at any site that has not responded to antibiotic therapy. In the United States one-fifth of tuberculosis occur at extra pulmonary sites. One third of human immunodeficiency virus (HIV)-infected individuals with tuberculosis have extra pulmonary disease with or without pulmonary involvement [7].

Fungal Osteomyelitis

Osteomyelitis can result from invasive infections due to a number of fungal pathogens,
including Candidaspecies. Sporothrixschenckii, Coccidioidesimmitis, Blastomycesdermitidis, Histoplasmacapsulatum, Cryptococcusneo formans, and variety of less commonly encountered pathogens. Fungal osteomyelitis should be considered in any indolent osteomyelitis that has not responded to routine measures or in any patient with evidence of disseminated fungal disease. Therapy is generally complex and prolonged .

Diabetic Foot Infections The organisms isolated are related in part to the severity of underlying disease, which has been divided into mild non –limb threatening infections and more severe limb-threatening infections [8]. Patients in
both groups frequently receive multiple courses of different antibiotics. Recent receipt of antibiotics increases the likely hood of atypical or drug-resistant organisms, particularly MRSA, but also enterococcus and Pseudomonas aeruginosa

Morphology

Acute Osteomyelitis

Bone destruction at sites of osteomyelitis are both the result of toxins produced by infecting microorganisms as well as the intense neutrophilic inflammation that occurs in response. Inflammation as well as the accompanying edema can result in significantly elevated intramedullary pressures, reducing blood supply, and in turn leading to ischemic necrosis of the involved bone. The pressurized focus of infection can also force its way to the bone cortex and ultimately under the periosteum which can separate from its underlying bone and in doing so compromise the bone's vascular supply, exacerbating ischemia and further contributing to bone ischemic necrosis. Particularly in children where bone and periosteum are loosely adhered, the infection can generate sub-periosteal abscesses or spread along sub-periosteal planes into adjacent joints. In adults, the infection can dissect through the periosteum and generate sinus tracts to the skin.

Chronic Osteomyelitis

Over time a chronic inflammatory infiltrate replaces the neutrophilic infiltrate of the acute phase. Pieces of dead necrotic bone, termed "sequestra" can be observed with shells of reactive bone forming around them, termed "involucra", representing a healing response aimed at isolating foci of infection from surrounding healthy bone. An involucrum can harbor viable organisms for years and also tends to render the affected bone structurally weaker, leading to a propensity for fracture. 

Complications

Osteomyelitis complications may include:

Bone death (osteonecrosis). An infection in your bone can impede blood circulation within the bone, leading to bone death. Areas where bone has died need to be surgically removed for antibiotics to be effective.

Septic arthritis. Sometimes, infection within bones can spread into a nearby joint.

Impaired growth. Normal growth in bones or joints in children may be affected if osteomyelitis occurs in the softer areas, called growth plates, at either end of the long bones of the arms and legs.

Skin cancer. If your osteomyelitis has resulted in an open sore that is draining pus, the surrounding skin is at higher risk of developing squamous cell cancer [10].

 

Treatment

Emergency Department Care

Osteomyelitis rarely requires emergent stabilization or resuscitation. The primary challenge for ED physicians is considering the appropriate diagnosis in the face of subtle signs or symptoms.

Treatment for osteomyelitis involves the following:

Initiation of intravenous antibiotics that penetrate bone and joint cavities

Referral of the patient to an orthopedist or general surgeon

Possible medical infectious disease consultation

Select the appropriate antibiotics using direct culture results in samples from the infected site, whenever possible. Empiric therapy is usually delayed until culture results can be obtained to better target definitive future antibiotic coverage. Empiric therapy is often initiated on the basis of the patient's age and the clinical presentation. Therapy should always include coverage for S aureus and consideration of CA-MRSA. Further surgical management may involve removal of the nidus of infection, implantation of antibiotic beads or pumps, hyperbaric oxygen therapy, [11] or other modalities.

 

Prognosis

The prognosis for osteomyelitis varies but is markedly improved with timely diagnosis and aggressive therapeutic intervention.

 

 

 

Referneces

 

Roy, M., Somerson, J. S., Kerr, K. G., & Conroy, J. L. (2012). Pathophysiology and pathogenesis of osteomyelitis. INTECH Open Access Publisher, 1-26.

Zimmerli W. Clinical practice. Vertebral osteomyelitis. N Engl J Med. 2010 Mar 18. 362(11):1022-9. 

Crary SE, Buchanan GR, Drake CE, Journeycake JM. Venous thrombosis and thromboembolism in children with osteomyelitis. J Pediatr. 2006 Oct. 149(4):537-41.

Kaplan SL. Osteomyelitis in children. Infect Dis Clin North Am. 2005 Dec. 19(4):787-97, vii

Chihara S, Segreti J. Osteomyelitis. Dis Mon. 2010 Jan. 56(1):5-31

6- Waldvogel FA, Medoff Swartz MN.(1970). Osteomyelitis: a review of clinical features,

therapeuticconsiderations, and unusual aspects. N. Engl J Med. 282:198-206.

7- Pineda C, Vargas A, Rodriguez AV. Imaging of osteomyelitis: current concepts (2006). Infect Dis N Am.

20:789-825

8- Cierny G 111, Mader J (1984). Adult chronic osteomyelitis. Orthopedics. 7(10):1557-64

 

9- Job-Deslandre C, Krebs S, Kahan A.(2001). Chronic recurrent multifocal osteomyelitis: Five years outcomes in

14 pediatric cases. Joint Bone Spine Rev Rheumatism. 68:245-251.

10- Overturf GD, Balfour G. Osteomyelitis and sepsis: severe complications of fetal monitoring. Pediatrics. 1975 Feb 1;55(2):244-7.

11- Kindwall EP. Uses of hyperbaric oxygen therapy in the 1990s. Cleve Clin J Med. 1992 Sep-Oct. 59(5):517-28.