Surgical Infections II – A. Osteomyelitis, Acute and Chronic


This Review is part of a series discussing the relationship of Human Infection and Surgery. Future Reviews in this series will deal with Septic Arthritis, Tuberculosis of Bones and Joints, Infections of specific body cavities, the surgical manifestations of HIV infection, wound infection and others.

Introduction  
General Principles of Bone and Joint Infections  
  Classification  
  Pathophysiology  
  Bacteriology  
  Diagnosis  
  Imaging  
Acute Osteomyelitis  
Sub-acute Osteomyelitis  
Chronic Osteomyelitis  
Post-trauma Osteomyelitis  
Recommendations  
Clinical cases
  Acute Hematogenous Osteomyelitis
  Chronic Osteomyelitis
  Post-trauma Osteomyelitis
References
Questions

 

Introduction
This Review must begin with a disclosure. I am not an orthopaedic surgeon and my orthopaedic experience has been limited to my surgical experiences in Africa. However these experiences have taught me that bone and joint infections are common in Africa; that they present late, often inadequately treated (1); are a major source of disability in all age groups, but primarily the young; present a challenge for the treating surgeon with limited means of diagnosis and with perhaps, like me, limited orthopaedic expertise. My experience is born out by the, unfortunately sparse, literature available from Africa. Bickler’s study (2) from the Gambia showed that, of all surgical conditions, cases of osteomyelitis alone accounted for 15% of total inpatient days, second only to burns. I have written this Review with that situation in mind.
I have relied heavily on the standard surgical literature on bone and joint infections (3 - 5), which is derived mostly from the developed world, but have focussed on the more common conditions seen in Africa. I discuss acute hematogenous osteomyelitis (AHO) and the chronic osteomyelitis (CO) that derives from it, as well as osteomyelitis that follows trauma and open fractures. I have omitted any discussion of infected prostheses and implants, although these represent a major problem in the developed world (6), or osteomyelitis involving the diabetic foot, which has specific characteristics. Finally I include photographs from my own experience, which illustrate some of the variety of bone infections.

General Principles of Bone and Joint Infections
Osteomyelitis can be classified into three major etiologic categories: 1. hematogenous, 2. exogenous from a contiguous infection or direct inoculum as in open fracture and 3. related to vascular insufficiency as in CO and when associated with diabetes. The disease is divided into acute, subacute or chronic based on the duration of symptoms and the presence of previous episodes. Major patient-related characteristics as in sickle cell anemia or HIV infection alter the response and character of infection. The Cierny-Mader classification incorporates both the anatomic extent of disease and patient characteristics and has been particularly useful in CO. (7)
The pathophysiology of osteomyelitis develops as a result of the particular anatomy and physiology of long bones. (8) The medullary cavity of bones, where hematogenous infection begins, is encased in a rigid structure, which does not allow for the expansion of the inflammatory process. Progression of the infection restricts medullary blood supply. Passage of pus through the cortex elevates the periosteum and the resulting sub-periosteal abscess causes bony infarction as the cortical bone is supplied by end-arteries from the periosteum. The necrotic bone acts as a persistent foreign body. Healing by periosteal new bone formation forms an involucrum, which further isolates the sequestrum from antibiotic therapy. Poor blood supply and necrotic bone account for the need for prolonged antibiotic therapy in AHO and the resistance of CO to therapy. Inflammation induces osteoclastic activity, which is partially responsible for the osteoporosis seen in x-rays of infected bone. The pathophysiology of post-trauma osteomyelitis shares some but not all of these characteristics. (9)
The growth and development of long bones from the epiphyseal plate also determines the characteristics of bony infection. Prior to 2 years of age, blood vessels cross the physis allowing the initial metaphyseal infection to spread into the epiphysis or even the joint. After 2 years, the developing plate restricts this and the infection tends to spread into the diaphysis of long bones. A recent study (10) found simultaneous septic joint involvement adjacent to an Osteomyelitis in as many as 1/3 of cases and also questioned this age distribution. Since the neck of the femur is essentially intra-articular, osteomyelitis here is always associated with septic arthritis. Untreated septic arthritis, involving particularly the intra-articular proximal femoral and humeral growth plates, can cause profound growth disturbances. With plate closure after puberty, hematogenous osteomyelitis becomes uncommon in adults, only to recur again in the elderly. (11)
Particular biochemical features also determine the bacteriology of osteomyelitis. Staphylococcus aureus possesses receptors, which facilitate its adherence to and invasion of bone and joint tissues. These may account for the fact that staph aureus constitutes the majority of endogenous infections. Osteomyelitis from staph aureus carrying the pvi gene appears to result in higher complications. (12) Streptococci are the second most common organisms, while specific vaccines against haemophilus influenzae have restricted this organism in those countries where they are used. (13) While most hematogenous infections are single agent, post-traumatic infections often yield multiple bacteria. Pseudomonas is a common pathogen, after puncture wounds of the foot. Patients with sickle cell anemia have an increased incidence of osteomyelitis caused by more frequently by salmonella agents. (14) Differentiating osteomyelitis from bone infarction, which requires only hydration and analgesia, is challenging. (15)
The diagnosis of bone or joint infection may be obvious or obscure. Fever, swelling and pain are the classic clinical triad; pain is the most persistent. Laboratory tests may or may not be positive. These include WBC count, ESR and C-reactive protein. The latter is probably the most sensitive, if not specific. (16) Blood culture may be positive in over 30% of cases of AHO. Aspiration of the medullary cavity, joint or direct bone biopsy, with culture, are the mainstays of certain diagnosis, are crucial in identifying the infecting agent and guide anti-microbial therapy. Gram stain may be positive in 30% of aspirates, but only culture is definitive. If no pus is identified a deep bone biopsy is necessary. (17) Aspiration cytology may be used to identify neoplastic lesions. (18) In acute infection blood or tissue culture is positive in 65% of cases. (19) Culture of sinus tracts in CO is misleading and only cultures of infected bone and soft tissue will reveal the causative agent. The fluid in septic arthritis generally has a cell count of more than 80,000 with more than 75% neutrophils, distinguishing septic arthritis from other causes of joint effusion.
A wide variety of imaging modalities have been developed for bone and joint infections. (20; 21) The plain x-ray may show bone destruction or periosteal new bone formation but not until 10-21 days after infection. Nuclear medicine scans are valuable for detecting inflammation. Technetium based bone scans are most sensitive and can detect osteomyelitis 48 hours after infection. Gallium and indium WBC scans have also been used. Trauma, recent surgery, the presence of prostheses; all lower the specificity of these tests. Ultrasound is particularly useful in identifying fluid collections in joints and around bone and is more likely to be available in African hospitals. (22) It may be used for aspirating infected areas. (23) CT scan and MRI are particularly useful in assessing degree of bony destruction, soft tissue extension and for specific regions. (24)

Acute Osteomyelitis
Acute hematogenous osteomyelitis (AHO) is a specific clinical entity affecting primarily children. Males are affected twice as often as females. While this disease is decreasing in frequency in the developed world (25), it is common throughout the developing world where it causes significant morbidity. Australian Aborigines and New Zealand Maoris experience a 7-10 fold increase in comparison to other children in the same countries. (26) A report from Lithuania (27) shows AHO increasing in frequency. Poverty, malnutrition, chronic disease, perhaps anemia, trauma and immuno-compromise are all compounding factors.
In Africa, where late presentation is the norm, the clinical picture is usually a febrile child with a swollen painful extremity s/he is resistant to use. Bony tenderness is characteristic. The differential diagnosis is cellulitis or pyomyositis, septic arthritis, bony infarction in a patient with sickle cell anemia, bony neoplasm, or other infectious diseases such as brucellosis, yaws, syphilis or leprosy. Septic arthritis, either alone or in combination with osteomyelitis is the most important differential diagnosis and is evaluated by aspiration of the joint.
X-rays and laboratory tests, including blood culture, should be done recognizing their limitations. U/S or nuclear scans may be useful if available.
The single most important investigative tool is aspiration of the involved tissue looking for pus and sending any material for culture and histology. A subperiosteal abscess represents a more advanced form of the disease. In its absence medullary aspiration or bone biopsy should be carried out.
In the absence of culture and sensitivity reports, empiric antibiotic therapy must be directed against all likely agents. Since staph aureus is the most common pathogen, a semi-synthetic penicillin, resistant to B-lactamase, such as cloxacillin is appropriate. (28) In situations where MRSA bacteria are common vancomycin, clindamycin, or rifampicin and an aminoglycoside may be necessary. Clindamycin achieves high bone concentrations. In children under 4 years, who have not been immunized against haemophilus influenzae, ampicillin should be added or ceftriaxone substituted.
The chief controversies in the management of AHO consist in the route and duration of antibiotic therapy (29) and the need for mandatory drainage of the involved bone.
The standard recommendation is for 4-6 weeks of antibiotic therapy, but this has been significantly reduced recently to 21 days. Unfortunately a meta-analysis showed that there are no high quality studies on which to base decisions. (30) One small RCT from Iran showed that in patients with AHO, who were responding to treatment and who continued on oral antibiotics for an additional 4 weeks, there were no differences between 10 or 21 days of intravenous therapy. (31) It should be further pointed out that all these patients had surgical drainage.
While it is well established that medullary pus and necrotic bone need to be surgically removed, the literature in developed countries recommends antibiotics as sole therapy, if initiated before the disease has progressed to this more advanced stage. Whether these recommendations are suitable for Africa is debatable. There is general agreement however that, if pus is found, the bone must be opened. Since blood supply derives from the periosteum, dissection should be limited. No less an authority than Primary Surgery is adamant on the need for drilling. (32) It states: “There is little point in aspirating it first, except sometimes to localise the site, because you will have to drill it anyway, even if the aspiration is negative”. King’s method is drilling as a diagnostic and therapeutic procedure and he gives a very good description of the technique. Drilling requires the placement of 3 to 4 holes staggered obliquely down the bone to prevent weakening. When intra-medullary pus is found, the Western literature recommends the creation of a cortical window with evacuation of pus and necrotic material. The limb is then splinted in plaster and mobilized after the wound has healed.
The point here is that pus from osteomyelitis must never go undrained and that, where possible, drainage should occur before the development of a subperiosteal abscess. While drilling and cortical windows have been associated with an increased risk of fracture, this may be due to the more advanced stage of the disease rather than the treatment itself. It is unlikely that the early cases described in Western literature are common in Africa. Under treatment or delayed treatment of AHO is associated with significant complications, the most significant being chronic osteomyelitis. (33) However with early treatment only 3% of patients will have long-term sequela.
AHO in adults more commonly involves the vertebrae than long bones. (34) Surgical treatment, which was required in over 60% of patients, requires specialized capability.

Sub-acute Osteomyelitis
Sub-acute osteomyelitis is a discrete clinical entity seen in the developed world and with increasing frequency. (35) It is felt to be a result of more indolent infection and is associated with specific radiographic abnormalities such as Brodie’s Abscess. (36) It must be distinguished from bony neoplasms. (37) In some cases these may indeed be indolent forms of infectious osteomyelitis (38 - 40); others may be the manifestations of chronic recurring multifocal osteomyelitis CRMO, which is a non-infectious condition of unknown etiology. (41) Aspiration or biopsy, culture and histology will resolve problems of diagnosis.

Chronic Osteomyelitis
The end stage of delayed or poorly treated AHO is chronic osteomyelitis (CO). Here, a chronic infection of the involved bone is perpetuated by the presence of a sequestrum, a necrotic piece of bone devascularized by the pathologic process described above. The sequestrum is surrounded by the involucrum, new bone formed by the periosteum. Indolent, recurrent, chronic infection is associated with sinus formation, pain and prolonged disability.
The diagnosis of CO is usually fairly obvious with a prior history of recurrent infections, disability and deformity arising after an initial event. However, Museru has stressed the necessity of distinguishing CO from bony neoplasms and, in this regard, bone biopsy is again the gold standard. (42) All the standard imaging techniques have been used to assess the extent of CO and to plan treatment. Sinogram is a simple technique, which can give information on the extent of disease. Bacteriologic diagnosis is important and can only be made with culture of bone. Effluent from sinus tracks is not a reliable indicator of the nature of the underlying infection.(43; 44) Interestingly staph aureus remains the main pathogen. (45)
The treatment of CO is multifaceted and complex. It involves: 1. the excision of all necrotic bone, 2. if necessary stabilization of the limb, 3.the application of appropriate, prolonged antibiotics, and 4.the obliteration of dead space through the closure and reconstruction of the soft tissue defect. (46) Multiple procedures are required. This applies equally to the treatment of posttraumatic osteomyelitis in the following section. The patient's general condition should be improved by correction of anemia or any nutritional deficiencies. There is seldom need for urgent intervention. Maurice King recommends delaying intervention until an adequate involucrum has formed to stabilize the limb. The recent literature from the developed world with its advanced orthopaedic techniques does not consider an inadequate involucrum a contraindication to debridement. The Cierny-Mader classification has been useful in assessing the degree of disease and the ability of the patient to respond to the treatment. Certainly some patients are better left without major intervention. A team approach has been associated with improved results. (47). The role of reconstructive efforts to improve local blood supply is important. (48)
There is a discrepancy between recent and older literature on the value of antibiotic therapy. Clearly, antibiotics are an adjunct to surgery and must be prolonged. The parenteral route is favoured. (49; 50) Various new oral agents including quinolones and linezolid are being investigated. (51; 52) Ciprofloxacin is a fluoroquinolone agent with excellent bone and soft tissue penetration and a broad spectrum of activity against gram positive organisms including staphylococci and gram negatives including pseudomonas. Extensive clinical use in pediatric populations with cystic fibrosis has not resulted in observed clinical toxicities and in particular the potential cartilage toxicity suggested by animal studies does not appear to be important in children. Because of its long half life once daily ceftriaxone has been used in an ambulatory setting. (53)
Surgical treatment begins with excision of all necrotic, infected bone. (54) The extent of excision has been correlated with success of treatment. (55) After adequate debridement, the medullary cavity is filled with a harvested autogenous bone graft. This is the Papineau technique. Posterior iliac bone grafts have lower complication rates than anterior grafts. (56) Alternatively local antibiotics in the form of bone cement or beads have been used. (57 - 59) Individual reports of the use of these methods show reasonable results. (60 - 62) No comparison can be made between techniques. When debridement results in instability of the limb temporary stabilization is achieved through immobilization in plaster, external fixation and even intramedullary nailing. Because the periosteum has been damaged, bony defects may have to be repaired through bone transfer (63) or the Ilizarov technique. (64 - 66)
Finally, soft tissue coverage of the defect is necessary to cover the bone and bring new blood supply to the region. (67) Sherman provides very good descriptions of some of the standard flaps, which are necessary to achieve closure of these wounds. For smaller indolent wounds with apparently healthy bone in their depths, I have found sugar to be a useful stimulant to closure. Hyperbaric oxygen has been used as an adjunctive method but the information on its efficacy is limited. (68)
The success rates for these techniques in eliminating infection and providing a functional limb vary between 50 and 90%. Considering the extent and difficulties of treatment, certain patients, in certain settings, are probably best left untreated. Amputation may occasionally be appropriate. Because of these difficulties, all attempts should be made to prevent CO by early and adequate treatment of AHO.
Certain regions and bones merit specific consideration. King gives a very good description of the approach to the major long bones and of the infection of specific regions.(32) Puncture wounds of the foot commonly give rise to osteomyelitis of tarsal and metatarsal bones, which usually require drainage or resection. (69) The calcaneus is a cancellous bone and so seldom forms a sequestrum or involucrum. Resection of all involved bone can be accomplished through a posterior midline incision with very good functional results. The fibula can be resected in its entirety if there is no infection of the tibia. (4) Infection of the distal third of the femur is difficult to treat and should be approached laterally with avoidance of the knee joint and neurovascular bundle. Conservative debridement is advised with splinting of the knee postoperatively. The ischial tuberosities are often involved in decubitus ulcers and prevent healing of these. Excision of involved bone and flap closure is required. When infected the entire ilium may be involved and may have to be resected. Jaw and skull infection have specific features.

Post-trauma Osteomyelitis
Post-trauma osteomyelitis (PTO) usually arises as a complication of open fracture. High velocity injuries associated with multiple bony devascularized fragments combined with major soft tissue loss are the frequent antecedents. (70; 71) Because of its poor soft tissue coverage, open fractures of the tibia are particularly susceptible to this complication. (72; 73) Delay in initiating treatment is a potent cause of complications. In Africa, traditional methods may delay modern treatment and are associated with complications. (74) In certain cases of mangled limbs, primary amputation may be appropriate.
The principles of open fracture treatment include: peri-operative short term antibiotics, urgent debridement of devitalized bone and soft-tissue, particularly muscle, copious irrigation of the wound, reduction and immobilization of fracture site, primary or delayed primary closure depending on the degree of contamination and soft tissue injury, early soft tissue closure, if necessary with flaps. (75) Various controversies exist and are beyond the scope of this Review. These include the degree of bony debridement, the use or avoidance of internal fixation, timing of wound closure, etc. Much of this is dependent on surgical expertise. A recent Cochrane Review confirmed the utility of peri-operative antibiotics in preventing infection with open fracture, but could not draw further conclusions. (76)
Once PTO has complicated the injury, treatment proceeds along similar lines discussed for CO.
Because of the nature of the bony injury and its associated complications such large bone defect, non- or mal-union of the fracture, advanced stabilization techniques, particularly external fixation, are more often required. Similarly advanced reconstructive techniques may be needed including free flaps. (77 - 80)
PTO and CO are some of the most challenging and difficult orthopaedic conditions. They are however, unfortunately common in the conditions of modern Africa.

Recommendations

  1. Direct aspiration of the involved bone for pus, culture and sensitivity and histology should always be carried out in patients at risk of acute hematogenous osteomyelitis (AHO). In children always consider the possibility of septic arthritis, which may occur separately or in the joint adjacent to AHO.
  2. Antibiotics active against staph aureus are the agents of choice in AHO. In children less than 4 years and not immunized against haemophilus, ampicillin should be added or ceftriaxone substituted.
  3. There is urgent need for high quality RCTs directed at the duration and route of antibiotic therapy for AHO and septic arthritis. In the absence of these one might recommend a minimum of 10-14 days intravenous therapy for responding patients followed by 4 weeks of oral therapy. Shorter regimes may produce similar results.
  4. Aspiration of bone for diagnosis and culture is mandatory in AHO. Finding pus requires drilling or the creation of a cortical window. Immediate drilling is another alternative.
  5. The Cierny-Mader classification should be used in the assessment of patients with chronic osteomyelitis (CO).
  6. The principles of treatment of CO are: 1.complete excision of all necrotic bone and sequestra, 2 stabilization of the limb, 3.appropriate and prolonged antibiotic therapy, 4.obliteration of all dead space and provision of increased blood supply through the reconstruction of the soft tissue and sometimes bony defect. In the absence of definitive superiority of the many techniques, surgeons should use those with which they are familiar. Treatment should be delayed until an adequate involucrum has been formed.
  7. A team approach, including orthopaedic and plastic surgeons, infectious disease specialists and dedicated nurses and physiotherapists, if available, gives superior results.
  8. The risk of post-trauma osteomyelitis (PTO) can be reduced through the judicious application of antibiotics and the principles of open fracture management.
  9. Wide debridement (>5mm) of necrotic and infected bone is associated with a lower risk of recurrence.
  10. Surgeons treating PTO should be familiar with a variety of techniques using muscle flaps for the closure of soft tissue defects.

Acknowledgement: I would like to thank Dr. Andrew Howard for reading an initial draft of this Review and making useful suggestions.

Brian Ostrow MD, FRCS(C)
Guelph, Ontario, Canada

Save review as .PDF

Click here to join the Surgery in Africa Discussion Group

Clinical cases
  Acute Hematogenous Osteomyelitis
  Chronic Osteomyelitis
  Post-trauma Osteomyelitis
  Questions

Reference List

  1. Onche II, Obiano SK. Chronic osteomyelitis of long bones: reasons for delay in presentation. Nigerian Journal of Medicine: Journal of the National Association of Resident Doctors of Nigeria 2004; 13(4):355-358. (123 kb)
  2. Bickler SW&BS. Epidemiology of paediatric surgical admissions to a government referral hospital in the Gambia. Bulletin of the World Health Organization 2000; 78(11):1330-1336. (277 kb)
  3. Cleveland K. General Principles of Infection. In: Canale, editor. Campbell's Operative Orthopaedics. St. Louis, MO: Mosby, Inc, 2003: 643-659. (306 kb)
  4. Dabov G. Osteomyelitis. In: Canale, editor. Campbell's Operative Orthopaedics. St. Louis MO: Mosby, Inc., 2003: 661-684. (657 kb)
  5. Berendt A&NC. Acute and Chronic Osteomyelitis. In: Cohen & Powderly, editor. Cohen & Powderly: Infectious Diseases. St. Louis Mo: Mosby, Inc., 2004: 571-582. (1 116 kb)
  6. Munoz P, Bouza E. Acute and chronic adult osteomyelitis and prosthesis-related infections. [Review] [44 refs]. Best Practice & Research in Clinical Rheumatology 1999; 13(1):129-147. (130 kb)
  7. Mader JT, Shirtliff M, Calhoun JH. The host and the skeletal infection: classification and pathogenesis of acute bacterial bone and joint sepsis. [Review] [63 refs]. Best Practice & Research in Clinical Rheumatology 1999; 13(1):1-20. (131 kb)
  8. Lazzarini L, Mader JT, Calhoun JH. Osteomyelitis in long bones. Journal of Bone & Joint Surgery - American Volume 2004; 86-A(10):2305-2318. (373 kb)
  9. Tsukayama DT. Pathophysiology of posttraumatic osteomyelitis. Clinical Orthopaedics & Related Research 1999;(360):22-29. (727 kb)
  10. Perlman MH, Patzakis MJ, Kumar PJ, Holtom P. The incidence of joint involvement with adjacent osteomyelitis in pediatric patients. Journal of Pediatric Orthopedics 2000; 20(1):40-43. (1 191 kb)
  11. Cunha BA. Osteomyelitis in elderly patients. Clinical Infectious Diseases 2002; 35(3):287-293. (97 kb)
  12. Martinez-Aguilar G, Avalos-Mishaan A, Hulten K, Hammerman W, Mason EO, Jr., Kaplan SL. Community-acquired, methicillin-resistant and methicillin-susceptible Staphylococcus aureus musculoskeletal infections in children.[see comment]. Pediatric Infectious Disease Journal 2004; 23(8):701-706. (118 kb)
  13. Howard AW, Viskontas D, Sabbagh C. Reduction in osteomyelitis and septic arthritis related to Haemophilus influenzae type B vaccination. Journal of Pediatric Orthopedics 1999; 19(6):705-709. (313 kb)
  14. Wong AL, Sakamoto KM, Johnson EE. Differentiating osteomyelitis from bone infarction in sickle cell disease. Pediatric Emergency Care 2001; 17(1):60-63. (66 kb)
  15. Skaggs DL, Kim SK, Greene NW, Harris D, Miller JH. Differentiation between bone infarction and acute osteomyelitis in children with sickle-cell disease with use of sequential radionuclide bone-marrow and bone scans. Journal of Bone & Joint Surgery - American Volume 2001; 83-A(12):1810-1813. (254 kb)
  16. Khachatourians AG, Patzakis MJ, Roidis N, Holtom PD. Laboratory monitoring in pediatric acute osteomyelitis and septic arthritis. Clinical Orthopaedics & Related Research 2003;(409):186-194. (214 kb)
  17. Carek PJ, Dickerson LM, Sack JL. Diagnosis and management of osteomyelitis.[erratum appears in Am Fam Physician 2002 May 1;65(9):1751]. [Review] [34 refs]. American Family Physician 2001; 63(12):2413-2420. (214 kb)
  18. Handa U, Bal A, Mohan H, Bhardwaj S. Fine needle aspiration cytology in the diagnosis of bone lesions. Cytopathology 2005; 16(2):59-64. (219 kb)
  19. Bonhoeffer J, Haeberle B, Schaad UB, Heininger U. Diagnosis of acute haematogenous osteomyelitis and septic arthritis: 20 years experience at the University Children's Hospital Basel. Swiss Medical Weekly 2001; 131(39-40):575-581. (243 kb)
  20. Santiago RC, Gimenez CR, McCarthy K. Imaging of osteomyelitis and musculoskeletal soft tissue infections: current concepts. [Review] [116 refs]. Rheumatic Diseases Clinics of North America 2003; 29(1):89-109. (364 kb)
  21. Oudjhane K, Azouz EM. Imaging of osteomyelitis in children. Radiologic Clinics of North America 2001; 39(2):251-266. (2 718 kb)
  22. Chau CL, Griffith JF. Musculoskeletal infections: ultrasound appearances. Clinical Radiology 2005; 60(2):149-159. (785 kb)
  23. Craig JG. Infection: ultrasound-guided procedures. Radiologic Clinics of North America 1999; 37(4):669-678. (1 831 kb)
  24. Kleinman PK. A regional approach to osteomyelitis of the lower extremities in children. Radiologic Clinics of North America 2002; 40(5):1033-1059. (1 222 kb)
  25. Blyth MJ, Kincaid R, Craigen MA, Bennet GC. The changing epidemiology of acute and subacute haematogenous osteomyelitis in children. Journal of Bone & Joint Surgery - British Volume 2001; 83(1):99-102. (340 kb)
  26. Steer AC, Carapetis JR. Acute hematogenous osteomyelitis in children: recognition and management. Paediatric Drugs 2004; 6(6):333-346. (433 kb)
  27. Malcius D, Trumpulyte G, Barauskas V, Kilda A. Two decades of acute hematogenous osteomyelitis in children: are there any changes? Pediatric Surgery International 2005; 21(5):356-359. (218 kb)
  28. Goergens ED, McEvoy A, Watson M, Barrett IR. Acute osteomyelitis and septic arthritis in children. Journal of Paediatrics & Child Health 2005; 41(1-2):59-62. (151 kb)
  29. Le Saux N, Howard A, Barrowman NJ, Gaboury I, Sampson M, Moher D. Shorter courses of parenteral antibiotic therapy do not appear to influence response rates for children with acute hematogenous osteomyelitis: a systematic review. BMC Infectious Diseases 2002; 2(1):16. (283 kb)
  30. Stengel D, Bauwens K, Sehouli J, Ekkernkamp A, Porzsolt F. Systematic review and meta-analysis of antibiotic therapy for bone and joint infections.[erratum appears in Lancet Infect Dis 2002 Feb;2(2):125]. The Lancet Infectious Diseases 2001; 1(3):175-188. (233 kb)
  31. Jaberi FM, Shahcheraghi GH, Ahadzadeh M. Short-term intravenous antibiotic treatment of acute hematogenous bone and joint infection in children: a prospective randomized trial. Journal of Pediatric Orthopedics 2002; 22(3):317-320. (121 kb)
  32. King M. Pus in Muscles, Bones, and Joints. In: King M, editor. Primary Surgery: Non-Trauma. Oxford: Oxford University Press, 1993: 83-103. (10 759 kb)
  33. Danielsson LG, Duppe H. Acute hematogenous osteomyelitis of the neck of the femur in children treated with drilling. Acta Orthopaedica Scandinavica 2002; 73(3):311-316. (406 kb)
  34. Rezai AR, Woo HH, Errico TJ, Cooper PR. Contemporary management of spinal osteomyelitis.[see comment]. Neurosurgery 1999; 44(5):1018-1025. (954 kb)
  35. Trobs R, Moritz R, Buhligen U, Bennek J, Handrick W, Hormann D et al. Changing pattern of osteomyelitis in infants and children. Pediatric Surgery International 1999; 15(5-6):363-372. (411 kb)
  36. Davies AM, Grimer R. The penumbra sign in subacute osteomyelitis. European Radiology 2005; 15(6):1268-1270. (133 kb)
  37. Shih HN, Shih LY, Wong YC. Diagnosis and treatment of subacute osteomyelitis. Journal of Trauma-Injury Infection & Critical Care 2005; 58(1):83-87. (196 kb)
  38. Rasool MN. Primary subacute haematogenous osteomyelitis in children. Journal of Bone & Joint Surgery - British Volume 2001; 83(1):93-98. (1 736 kb)
  39. Auh JS, Binns HJ, Katz BZ. Retrospective assessment of subacute or chronic osteomyelitis in children and young adults. Clinical Pediatrics 2004; 43(6):549-555. (700 kb)
  40. Gonzalez-Lopez JL, Soleto-Martin FJ, Cubillo-Martin A, Lopez-Valverde S, Cervera-Bravo P, Navascues del Rio JA et al. Subacute osteomyelitis in children. Journal of Pediatric Orthopaedics, Part B 2001; 10(2):101-104. (88 kb)
  41. Girschick HJ, Raab P, Surbaum S, Trusen A, Kirschner S, Schneider P et al. Chronic non-bacterial osteomyelitis in children. Annals of the Rheumatic Diseases 2005; 64(2):279-285. (429 kb)
  42. Museru LM, Mcharo CN. Chronic osteomyelitis: a continuing orthopaedic challenge in developing countries. International Orthopaedics 2001; 25(2):127-131. (95 kb)
  43. Zuluaga AF, Galvis W, Jaimes F, Vesga O. Lack of microbiological concordance between bone and non-bone specimens in chronic osteomyelitis: an observational study. BMC Infectious Diseases 2002; 2(1):8. (225 kb)
  44. Agarwal S, Zahid M, Sherwani MK, Abbas M, Huda N, Khan AQ. Comparison of the results of sinus track culture and sequestrum culture in chronic osteomyelitis. Acta Orthopaedica Belgica 2005; 71(2):209-212. (91 kb)
  45. Yeargan SA, III, Nakasone CK, Shaieb MD, Montgomery WP, Reinker KA. Treatment of chronic osteomyelitis in children resistant to previous therapy. Journal of Pediatric Orthopedics 2004; 24(1):109-122. (500 kb)
  46. Parsons B, Strauss E. Surgical management of chronic osteomyelitis. American Journal of Surgery 2004; 188(1A Suppl):57-66. (599 kb)
  47. Ziran BH, Rao N, Hall RA. A dedicated team approach enhances outcomes of osteomyelitis treatment. Clinical Orthopaedics & Related Research 2003;(414):31-36. (151 kb)
  48. Hausman MR, Rinker BD. Intractable wounds and infections: the role of impaired vascularity and advanced surgical methods for treatment. American Journal of Surgery 2004; 187(5A):44S-55S. (1 295 kb)
  49. Mader JT, Shirtliff ME, Bergquist SC, Calhoun J. Antimicrobial treatment of chronic osteomyelitis. Clinical Orthopaedics & Related Research 1999;(360):47-65. (1 548 kb)
  50. Shuford JA, Steckelberg JM. Role of oral antimicrobial therapy in the management of osteomyelitis. Current Opinion in Infectious Diseases 2003; 16(6):515-519. (93 kb)
  51. Greenberg RN, Newman MT, Shariaty S, Pectol RW. Ciprofloxacin, lomefloxacin, or levofloxacin as treatment for chronic osteomyelitis. Antimicrobial Agents & Chemotherapy 2000; 44(1):164-166. (42 kb)
  52. Rao N, Ziran BH, Hall RA, Santa ER. Successful treatment of chronic bone and joint infections with oral linezolid. Clinical Orthopaedics & Related Research 2004;(427):67-71. (70 kb)
  53. Guglielmo BJ, Luber AD, Paletta D, Jr., Jacobs RA. Ceftriaxone therapy for staphylococcal osteomyelitis: a review. Clinical Infectious Diseases 2000; 30(1):205-207. (59 kb)
  54. Tetsworth K, Cierny G, III. Osteomyelitis debridement techniques. [Review] [38 refs]. Clinical Orthopaedics & Related Research 1999;(360):87-96. (836 kb)
  55. Simpson AH, Deakin M, Latham JM. Chronic osteomyelitis. The effect of the extent of surgical resection on infection-free survival. Journal of Bone & Joint Surgery - British Volume 2001; 83(3):403-407. (300 kb)
  56. Ahlmann E, Patzakis M, Roidis N, Shepherd L, Holtom P. Comparison of anterior and posterior iliac crest bone grafts in terms of harvest-site morbidity and functional outcomes. Journal of Bone & Joint Surgery - American Volume 2002; 84-A(5):716-720. (91 kb)
  57. Zalavras CG, Patzakis MJ, Holtom P. Local antibiotic therapy in the treatment of open fractures and osteomyelitis. Clinical Orthopaedics & Related Research 2004;(427):86-93. (132 kb)
  58. Klemm K. The use of antibiotic-containing bead chains in the treatment of chronic bone infections. Clinical Microbiology & Infection 2001; 7(1):28-31. (271 kb)
  59. Kanellakopoulou K, Giamarellos-Bourboulis EJ. Carrier systems for the local delivery of antibiotics in bone infections. Drugs 2000; 59(6):1223-1232. (125 kb)
  60. Alonge TO, Ogunlade SO, Omololu AB. The Belfast technique for the treatment of chronic osteomyelitis in a tropical teaching hospital. International Orthopaedics 2003; 27(2):125-128. (113 kb)
  61. Hashmi MA, Norman P, Saleh M. The management of chronic osteomyelitis using the Lautenbach method. Journal of Bone & Joint Surgery - British Volume 2004; 86(2):269-275. (125 kb)
  62. Pelissier P, Boireau P, Martin D, Baudet J. Bone reconstruction of the lower extremity: complications and outcomes. Plastic & Reconstructive Surgery 2003; 111(7):2223-2229. (194 kb)
  63. Steinlechner CW, Mkandawire NC. Non-vascularised fibular transfer in the management of defects of long bones after sequestrectomy in children. Journal of Bone & Joint Surgery - British Volume 2005; 87(9):1259-1263. (563 kb)
  64. Kucukkaya M, Kabukcuoglu Y, Tezer M, Kuzgun U. Management of childhood chronic tibial osteomyelitis with the Ilizarov method. Journal of Pediatric Orthopedics 2002; 22(5):632-637. (471 kb)
  65. Emara KM. Hemi-corticotomy in the management of chronic osteomyelitis of the tibia. International Orthopaedics 2002; 26(5):310-313. (144 kb)
  66. Barbarossa V, Matkovic BR, Vucic N, Bielen M, Gluhinic M. Treatment of osteomyelitis and infected non-union of the femur by a modified Ilizarov technique: follow-up study. Croatian Medical Journal 2001; 42(6):634-641. (138 kb)
  67. Sherman R. Soft Tissue Coverage. In: Browner BD, editor. Skeletal Trauma: Basic Science, Management, and Reconstruction. Saunders, 2003: 320-348. (1 904 kb)
  68. Wang C, Schwaitzberg S, Berliner E, Zarin DA, Lau J. Hyperbaric oxygen for treating wounds: a systematic review of the literature. Archives of Surgery 2003; 138(3):272-279. (104 kb)
  69. Ansari MA, Shukla VK. Foot infections. International Journal of Lower Extremity Wounds 2005; 4(2):74-87. (146 kb)
  70. Mader JT, Cripps MW, Calhoun JH. Adult posttraumatic osteomyelitis of the tibia. Clinical Orthopaedics & Related Research 1999;(360):14-21. (644 kb)
  71. Holtom PD, Smith AM. Introduction to adult posttraumatic osteomyelitis of the tibia. Clinical Orthopaedics & Related Research 1999;(360):6-13. (675 kb)
  72. Ikem IC, Oginni LM, Bamgboye EA. Open fractures of the lower limb in Nigeria. International Orthopaedics 2001; 25(6):386-388. (26 kb)
  73. Beals RK, Bryant RE. The treatment of chronic open osteomyelitis of the tibia in adults. Clinical Orthopaedics & Related Research 2005;(433):212-217. (122 kb)
  74. Alonge TO, Dongo AE, Nottidge TE, Omololu AB, Ogunlade SO. Traditional bonesetters in south western Nigeria--friends or foes? West African Journal of Medicine 2004; 23(1):81-84. (110 kb)
  75. Wood II G. General Principles of Fracture Treatment. In: Canale R, editor. Canale: Campbell's Operative Orthopaedics. St. Louis MO: Mosby Inc., 2003: 2669-2693. (339 kb)
  76. Gosselin RA, Roberts I, Gillespie WJ. Antibiotics for preventing infection in open limb fractures. Cochrane Database of Systematic Reviews 2004;(1):CD003764. (289 kb)
  77. Gonzalez MH, Weinzweig N. Muscle flaps in the treatment of osteomyelitis of the lower extremity. Journal of Trauma-Injury Infection & Critical Care 2005; 58(5):1019-1023. (99 kb)
  78. Gonzalez MH, Tarandy DI, Troy D, Phillips D, Weinzweig N. Free tissue coverage of chronic traumatic wounds of the lower leg. Plastic & Reconstructive Surgery 2002; 109(2):592-600. (66 kb)
  79. Hong JP, Shin HW, Kim JJ, Wei FC, Chung YK. The use of anterolateral thigh perforator flaps in chronic osteomyelitis of the lower extremity. Plastic & Reconstructive Surgery 2005; 115(1):142-147. (167 kb)
  80. Necmioglu S, Askar I, Lok V, Subasi M. Use of the vastus lateralis muscle flap with a grooving procedure in the surgical treatment of chronic osteomyelitis of the femur. Annals of Plastic Surgery 2004; 53(6):570-576. (279 kb)

Save review as .PDF

Questions

Click here to join the Surgery in Africa Discussion Group

(Back to Top)

Previous Review
Surgery in Africa Home
Next Review