Osteomyelitis In Adults


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  • Osteomyelitis In Adults

    2. 2. OSTEOMYELITIS <ul><li>Nelaton (1834): coined osteomyelitis </li></ul><ul><li>The root words osteon (bone) and myelo (marrow) are combined with itis (inflammation) to define the clinical state in which bone is infected with microorganisms. </li></ul>
    3. 3. CLASSIFICATION <ul><li>The two most widely used in the medical literature and in clinical practice are those presented by </li></ul><ul><li>Waldvogel et al </li></ul><ul><li>Cierny et al. </li></ul>
    4. 4. WALDVOGEL CLASSIFICATION <ul><li>According to the duration of the disease </li></ul><ul><ul><li>acute </li></ul></ul><ul><ul><li>chronic </li></ul></ul><ul><li>On the basis of the pathogenesis </li></ul><ul><ul><li>hematogenous </li></ul></ul><ul><ul><li>secondary to a contiguous focus of infection </li></ul></ul><ul><ul><li>associated with peripheral vascular disease </li></ul></ul>
    5. 5. ACUTE / CHRONIC OM <ul><li>The term acute osteomyelitis is used clinically to signify a newly recognized bone infection. Patients usually present within several days to one week after the onset of symptoms. In addition to local signs of inflammation and infection, patients have signs of systemic illness </li></ul><ul><li>The relapse of a previously treated or untreated infection is considered a sign of chronic disease . Clinical signs persisting for more than 10 days correlate roughly with the development of necrotic bone and chronic osteomyelitis. The clinical pattern may evolve over months or even years and is characterized by lowgrade inflammation; the presenceof pus, microorganisms,and sequestra; a compromised soft-tissue envelope;and sometimes a fistula. </li></ul>
    6. 6. HEMATOGENOUS OM – Follows Bacteremia <ul><li>Usually occurs in </li></ul><ul><li>Children – long bones, usually of lower extremities </li></ul><ul><li>Middle aged adults who use IV Drugs – Vertebrea, Pubic Symphysis, Sternoclavicular & Sacroiliac joints </li></ul><ul><li>Elderly – Vertebrea </li></ul><ul><li>Predisposing factors include any cause of persistent bacteremia </li></ul><ul><li>central venous catheter infections </li></ul><ul><li>endocarditis </li></ul><ul><li>hemoglobinopathies such as sickle cell disease </li></ul><ul><li>immunodeficiency states chronic granulomatous disease </li></ul><ul><li>Clinical Features </li></ul><ul><li>Children - fever, evidence of inflammation including pain at the involved site, erythema, warmth, and induration; Blood cultures are often positive </li></ul><ul><li>Adults – course is often more indolent </li></ul><ul><li>Pain is the common manifestation </li></ul><ul><li>Only about half of adults with vertebral osteomyelitis have a fever. </li></ul><ul><li>Percussion tenderness and paraspinal muscle tenderness is more common, and the disease may progress to paraparesis or paraplegia. </li></ul><ul><li>Blood cultures are often negative, so needle biopsy with multiple specimens for microbiologic and pathological examination is the diagnostic procedure of choice </li></ul>
    7. 7. … .HEMATOGENOUS OM (cont.) <ul><li>Etiology </li></ul><ul><li>Usually caused by only a single microbial species </li></ul><ul><li>in over 50% of cases, the organism is Staphylococcus aureus </li></ul><ul><li>OM in intravenous drug users is often secondary to Pseudomonas aeruginosa </li></ul><ul><li>Elderly adults with vertebral osteomyelitis may have infections due to gram-negative urinary pathogens. </li></ul><ul><li>Neonates are predisposed to infections from group B streptococci or gram-negative bacilli. </li></ul><ul><li>Patients with sickle-cell disease, often have infections due to Salmonella. </li></ul><ul><li>Mycobact Tuberculosis (Pott’s disease) </li></ul><ul><li>Brucellosis due to exposure to cattle, sheep, goats, pigs, or consumption of unpasteurized dairy products; </li></ul><ul><li>Coxiella burnetii associated with farm animals </li></ul><ul><li>The endemic fungi such as Blastomyces dermatitidis or Coccidiodes immitis; and atypical mycobacteria or Bartonella henselae in patients with HIV disease. </li></ul><ul><li>Patients who are immunosuppressed and have central venous catheters may have infections due to opportunistic fungi such as Candida, Aspergillus, or Rhizopus. </li></ul>
    8. 8. OM SECONDARY TO A CONTIGUOUS FOCUS OF INFECTION <ul><li>Direct infection of a bone from an exogenous source </li></ul><ul><li>Extension of an infection from a contiguous focus </li></ul><ul><li>This is the most common OM in adults. </li></ul><ul><li>The long bones of the extremities, such as the tibia and femur, are the most common sites of involvement. </li></ul><ul><li>Clinical Features - Patients usually present with only local symptoms of erythema, swelling, and pain. As the infection becomes more chronic, persistent purulent sinus-tract drainage forms. Most patients do not have a fever, leukocytosis, or an elevated ESR </li></ul>
    9. 9. … OM SECONDARY TO A CONTIGUOUS FOCUS OF INFECTION <ul><li>Etiology </li></ul><ul><li>Infection is polymicrobial in 30% to 50% of cases and blood cultures are unlikely to be positive </li></ul><ul><li>S. aureus remains the most likely pathogen </li></ul><ul><li>Aerobic gram-negative bacilli can be found in 30% of cases. </li></ul><ul><li>Anaerobic organisms should be suspected following bites, extensions of dental or sinus infections, or associated with decubitus ulcers, especially of the sacrum or pelvic bones. </li></ul><ul><li>Infections associated with cat bites are often due to Pasteurella multocida, while human bite infections may involve Eikenella corrodens. </li></ul><ul><li>P. aeruginosa is associated with foot osteomyelitis after puncture wounds in wearers of sneakers. </li></ul><ul><li>Staphylococcus epidermidis is a likely pathogen associated with infections associated with orthopedic hardware devices,such as plates, rods, or prosthetic joints. </li></ul>
    10. 10. OM ASSOCIATED WITH PERIPHERAL VASCULAR DISEASE <ul><li>Found almost exclusively in the feet in patients with a long history of diabetes mellitus and peripheral neuropathy. </li></ul><ul><li>Bone involvement usually occurs after an extension of soft tissue infection involving a plantar ulcer. </li></ul><ul><li>Clinical Features </li></ul><ul><li>erythema and drainage </li></ul><ul><li>either no pain (if there is advanced neuropathy) or excruciating pain (if the destruction of bone has been acute). </li></ul><ul><li>patients are afebrile, </li></ul><ul><li>present with an ulcer without evidence of surrounding inflammation. The ulcer size (> 2 cm 2 ) and depth (> 3 mm) are predictive of the likelihood of bone involvement. If bone can be felt with a sterile blunt probe, the likelihood of osteomyelitis is high. </li></ul><ul><li>a high ESR, especially if it is over 70 mm/hour, is helpful in making the diagnosis of osteomyelitis </li></ul>
    11. 11. … OM ASSOCIATED WITH PERIPHERAL VASCULAR DISEASE <ul><li>ETIOLOGY </li></ul><ul><li>Most infections are polymicrobial </li></ul><ul><li>S. aureus remains the most common pathogen </li></ul><ul><li>others include Enterococcus faecalis, group B streptococci, Enterobacteriaceae, anaerobic bacteria (especially peptococci, peptostreptococci, and Bacteroides species), and P. aeruginosa </li></ul>
    12. 12. CIERNY-MADER STAGING SYSTEM FOR OSTEOMYELITIS The Cierny-Mader system classifies osteomyelitis on the degree of anatomic involvement and the physiologic features of the host and has been helpful in stratifying treatment and prognosis for long bone infections. The stages in this system are dynamic and may be altered by changes in the medical condition of the patient (host), successful antibiotic therapy and other treatments. Anatomic type Stage 1: Medullary osteomyelitis - Confined to medullary cavity, examples include hematogenous osteomyelitis or associated with intramedullary rods Stage 2: Superficial osteomyelitis - Exposed infected bone at the base of a wound Stage 3: Localized osteomyelitis - Full thickness cortical sequestration that can be removed without compromising stability Stage 4: Diffuse osteomyelitis - Involvement of both cortex and medullary cavity associated with loss of stability
    13. 13. Physiologic class A host: healthy & has no systemic or local compromising factors B host: is affected by one or more compromising factors Bs: systemic compromise - Malnutrition, renal or hepatic failure, diabetes, chronic hypoxia, immune deficiency, malignancy, extremes of age Bl: local compromise - Chronic lymphedema, venous stasis, major vessel compromise, arteritis, extensive scarring, radiation fibrosis, small-vessel diseases, neuropathy, tobacco abuse Bls: local and systemic compromise C host: Treatment worse than the disease. The host is so severely compromised that the radical treatment necessary would have an unacceptable risk-benefit ratio. Suppressive antibiotic therapy and/or amputation recommended The anatomical & physiological classes are combined to designate 1 of 12 clinical stages of osteomyelitis. Eg. A type II lesion in a class A host is designated as stage IIA OM. This system is helpful in determining if t/t should be simple /complex, curative/palliative, limb sparing/ablative … CIERNY-MADER STAGING SYSTEM FOR OSTEOMYELITIS (cont.)
    14. 14. PATHOGENESIS Infection Inflammatory response Phagocytes attempt to contain infection by liberating enzymes enzymes lyse the bone pus forms pus travels through haversian system increased intra osseous pressure endarteritis and impaired blood flow ischemic necrosis of bone pus breaks through the cortex
    15. 15. abscesses subperiosteal / soft tissue elevated periosteum- deposits new bone ( involucrum ) sites of rupture of periosteum – (cloacae) This process may take several months and may get halted at any stage depending upon the host resistance and virulence of infecting organisms If infection gets completely eradicated, the necrosed bone does not separate but is gradually replaced by process of creeping substitution
    16. 16. Sequestrum : is a devitalized avascular segment of bone, surrounded, by pus /infected granulation tissue and is more dense than surrounding bone .Because of avascularity , sequestrum does not decalcify , is more radio opaque and heavy , so sinks in water Its outer surface is usually jagged / irregular due to erosive process by proteolytic enzymes in granulation tissue Types of Sequestra : 1 Tubular ( Diaphyseal) – Pyogenic Osteomyelitis 2 Trapezoid - Pyogenic Osteomyelitis 3 Ring -At end of stumps, around Steinman pin, wires, Schanz screws 4 Flake/ Feathery - Tuberculous Osteomyelitis( in cavity ) 5 coarse sandy - Tuberculous Osteomyelitis ( out of cavity ) 6 Fine sandy - Viral Osteomyelitis 7 Black - Actinomycosis
    17. 17. .) Involucrum : is derived from the word “volvere” i.e. to wrap .It is the result of reactive new bone formed by periosteal reaction , in an attempt to wall off the infection by forming a thick tense wall It is jagged on its inner surface but smooth on its outer surface Cloacae : are single or multiple openings in involucrum and are caused by rupture of periosteum due to pus under tension . Exudates , sequestra are extruded through the cloacae on the surface
    18. 18. <ul><li>Important factors in the pathogenesis of osteomyelitis </li></ul><ul><li>In the early stages of colonization, bacteria can still be killed or contained by host defences. But they can remain viable when Inoculum is larger than threshold levels Host defences are impaired Tissue on which bacteria colonizes is traumatized or necrotic A foreign body is present Surface is acellular or inanimate (dead bone, cartilage, biomaterials) </li></ul><ul><li>Formation of glycocalyx by the bacteria surrounding the infecting organisms. This glycocalyx protects the organisms from the action of phagocytes and prevents access by most antimicrobials. The biofilms are community of metabolically inactive bacteria & will only form on inert or nonviable surfaces. </li></ul><ul><li>Gaining access to the interior of cells that may contribute to the understanding of the persistence and flare-ups of osteomyelitis. </li></ul>
    19. 19. chronic osteomyelitis(contd.) The diagnosis of osteomyelitis is based on clinical examination, imaging and laboratory studies. The gold standard is to take biopsy for histopathology and microbiological evaluation
    20. 20. <ul><li>LABORATORY STUDIES </li></ul><ul><li>Leucocyte count </li></ul><ul><li> Increase – Acute OM </li></ul><ul><li> Normal – Chronic OM </li></ul><ul><li>2. ESR – Peak elevation of ESR occurs at 3 to 5 days after infection and returns to normal after about 3 weeks after treatment is started </li></ul><ul><li>Persistently increase ESR after treatment in a compromise host – a reason other than OM </li></ul><ul><li>Not Diagnostic however return of ESR to normal in course of t/t is a favorable prognostic sign </li></ul>
    21. 21. <ul><li>3. C-Reactive protein </li></ul><ul><li>Increase in both acute and chronic OM. </li></ul><ul><li>Decrease faster than ESR. </li></ul><ul><li>More sensitive than ESR. </li></ul><ul><li>CRP increases within 6 hrs of infection, reaches a peak elevation 2 days after infection and returns to normal within one week after adequate treatment has begun </li></ul><ul><li>4. Serum Creatinine level – To monitor drug toxicity </li></ul><ul><li>5. LFT – To monitor drug toxicity </li></ul><ul><li>6. Serum albumin level – For nutritional status </li></ul><ul><li>7. Total iron binding capacity – For nutritional status </li></ul>
    22. 22. R A D I O G R A P H I C D I A G N O S I S O F O S T E O M Y E L I T I S <ul><li>No radiographic technique can make or exclude a diagnosis of osteomyelitis with certainty. </li></ul><ul><li>Plain film Radiographs </li></ul><ul><li>lag at least two weeks behind the process of infection </li></ul><ul><li>The earliest changes are swelling of the soft tissue, periosteal thickening and/or elevation, and focal osteopenia. </li></ul><ul><li>The more diagnostic lytic changes are delayed and are associated with subacute and chronic osteomyelitis. </li></ul><ul><li>Osteoporosis is a feature of metabolically active living bone; the segment that fails to become osteoporotic is metablically inactive and possibly dead. </li></ul><ul><li>Sinography can be performed if a sinus track is present and can be a valuable adjunct to surgical planning. </li></ul>
    23. 23. <ul><li>2. Ultrasound – may detect a subperiosteal collection of fluid in early stages of osteomyelitis . </li></ul><ul><li>3. Computarized Tomograhy - is particularly helpful in </li></ul><ul><li>detecting smaller areas of cortical destruction, </li></ul><ul><li>Small foci of gas or foreign bodies, </li></ul><ul><li>sequestra formation (areas of necrotic bone separated by granulation tissue from living bone) </li></ul><ul><li>involucra (a layer ofliving bone that has formed along the sequestrum), </li></ul><ul><li>cloacae (an opening in the involucrum through which the sequestrum and granulation tissue may be discharged) </li></ul><ul><li>surrounding soft-tissue abscesses and </li></ul><ul><li>the replacement of the normal bone marrow fat with pus. </li></ul><ul><li>These features often predict the need for surgical debridement, and therefore can be helpful in planning and determining the need for surgical therapy. </li></ul><ul><li>One disadvantage of this study is the scatter phenomenon, which occurs when metal is present in or near the area of bone infection and results in a substantial loss of image resolution. </li></ul>
    24. 24. <ul><li>4. Magnetic resonance imaging </li></ul><ul><li>MRI has very high sensitivity and specificity for the diagnosis of osteomyelitis. </li></ul><ul><li>The typical appearance is a localized area of abnormal marrow with decreased signal intensity on T1-weighted images and increased signal intensity on T2-weighted images. </li></ul><ul><li>Sinus tracts are seen as areas of high signal intensity extending from the marrow and bone through the soft tissues and through the skin on T2-weighted images </li></ul><ul><li>Useful for differentiating between bone and soft-tissue infection, which is often a problem with radionuclide studies. </li></ul><ul><li>Unlike radionuclide studies, magnetic resonance imaging is not useful for whole-body examinations. </li></ul><ul><li>Also, a metallic implant in the region of interest may produce focal artifacts, thereby decreasing image quality </li></ul><ul><li>The intravenous contrast agent gadopentetate di- N -methylglucamine, a paramagneticmaterial, may also be useful in differentiating vascularized and inflamed tissue from the peripheralrim enhancement characteristic of an abscess </li></ul>
    25. 25. 5. Radionuclide Scans <ul><li>Performed when the diagnosis of osteomyelitis is ambiguous or to help gauge the extent of bone and soft-tissue inflammation. </li></ul><ul><li>Technetium-99m methylene diphosphonate bone scanning can detect abnormalities as early as 24–48 hours, and are almost always positive by 8 days. Osteomyelitis causes increased uptake in all the three phases (flow phase, equilibruim phase and delayed phase) </li></ul><ul><li>A technetium-99m scan may be negative for a patient with documented osteomyelitis because of a decrease in blood flow to the infected area (subperiosteal pus, sequestrum, joint effusion, vasospasm, soft tissue swelling) </li></ul><ul><li>Trauma, arthritis, overlaying cellulitis, tumor, synovitis, or the neuropathic osteoarthropathy commonly observed in the feet of diabetic patients can cause false-positive scans. </li></ul><ul><li>A gallium67 citrate scan, which accumulates in inflammatory sites, is generally sensitive but not specific in the diagnosis of osteomyelitis, because overlaying cellulitis, inflammatory arthritis, tumors, hematomas, neuropathic osteoarthropathy, and fractures can also cause positive scans </li></ul>
    26. 26. … Radionuclide Scans <ul><li>Indium111-labelled leukocyte scans, although likely more specific than bone scanning, can be false-positive in patients with cellulitis or other inflammatory conditions, and can be false-negative in chronic infections. </li></ul><ul><li>To enhance spatial resolution, gallium or indium scanning is sometimes combined with bone scanning, which increases not only the cost but also the time of obtaining the results. </li></ul>
    27. 27. M I C R O B I O L O G I C D I A G N O S I S O F O S T E O M Y E L I T I S <ul><li>Key to the successful management of osteomyelitis is the isolation of the involved pathogens before the initiation of antibiotics in order to tailor optimal antimicrobial therapy </li></ul><ul><li>In acute osteomyelitis, especially in children, blood cultures are positive in more than half of patients </li></ul><ul><li>In patients with acute hematogenous osteomyelitis of long bones, a needle aspirate is often performed. If subperiosteal pus is found, it is cultured; if not, the needle is inserted into the marrow cavity and an aspirate is performed </li></ul><ul><li>Patients with vertebral osteomyelitis who do not require immediate surgical therapy should have a closed biopsy of the bone performed, often under radiographic guidance. If the biopsy is negative, it should be repeated, using either a closed or open technique. If 2 closed-needle biopsies are negative, open surgical biopsy should be undertaken. </li></ul>
    28. 28. ......M I C R O B I O L O G I C D I A G N O S I S O F O S T E O M Y E L I T I S <ul><li>Patients with chronic osteomyelitis frequently have draining sinus tracts. Culture of material fromthe sinus tracts do not necessarily reflect the pathogens that are infecting the bone. However, growth of S. aureus in pure culture from the tract does have a high predictive value for its presence in bone. The most reliable specimens are biopsies ofthe bone material. </li></ul><ul><li>The best way to make a microbiologic diagnosis is with either an open or a needle biopsy, but open biopsies are invasive, and needle biopsies may be false-negative due to sampling errors. </li></ul><ul><li>Culture swabs of grossly purulent material, curettage, or needle aspirates of the ulcer base can also be performed, because bone infections are usually an extension of the soft tissue infection. </li></ul>
    29. 29. TREATMENT <ul><li>If osteomyelitis is suspected on clinical grounds, blood and fluid samples should be taken and then treatment should be started immediately without waiting for final confirmation of the diagnosis. </li></ul><ul><li>Four important aspects for the management of the patient </li></ul><ul><li>Supportive treatment for pain and dehydration </li></ul><ul><li>Splintage of the affected part </li></ul><ul><li>3. If the patient is a compromised host, an effort is made to correct or reduce the host defect or defects. In particular, attention should be paid togood nutrition, to a smoking cessation program, and to controlof specific diseases such as diabetes. Thus, an attempt is made to improve the nutritional, medical, and vascular statusof the patient and to provide optimal treatment of any underlying disease. </li></ul><ul><li>4. Antimicrobial therapy </li></ul><ul><li>5. Surgical procedures </li></ul>
    30. 30. … treatment (cont.) <ul><li>NADE’S Principles </li></ul><ul><li>an appropriate antibiotic will b effective before pus formation </li></ul><ul><li>Antibiotics will not sterilize avascular tissues or abscess and such areas require surgical removal </li></ul><ul><li>If such removal is effective, antibiotics should prevent there reformation and therefore primary wound closure should be safe. </li></ul><ul><li>Surgery should not further damage already ischeamic bone and soft tissue. </li></ul><ul><li>Antibiotics should be continued after surgery. </li></ul>
    31. 31. … treatment (cont.) ANTIMICROBIAL THERAPY <ul><li>Ideally, the treatment of osteomyelitis should be based on the results of bone cultures. After culture specimens are obtained by means of a bone biopsy or during débridement, a parenteral antimicrobial regimen is begun to cover the clinically suspected pathogens. Once the organism is identified, the treatment may be modified according to the sensitivity of the isolated microorganisms </li></ul><ul><li>Length of therapy - The traditional duration of treatment in most stages of osteomyelitis (Cierny-Mader Stages 1, 3, and 4) is four to six weeks. The rationale for this duration is based on the observation that revascularization of bone after débridement takes about four weeks. </li></ul><ul><li>Parenteral versus oral therapy - The decision to use oral rather than parenteral antibiotics should be based on results regarding microorganism sensitivity, patient compliance, infectious disease consultation, and the surgeon’s experience. The drugs of proven efficacy in the oral treatment of osteomyelitis are clindamycin, rifampin, cotrimoxazole, and fluoroquinolones </li></ul><ul><li>The role of synergistic or combination antimicrobial therapy - Oral rifampin is currently used as a combination drug in both parenteral and oral regimens for Staphylococcus aureus infections. Rifampin kills intracellular organisms. </li></ul>
    32. 32. … treatment (cont.) ANTIMICROBIAL THERAPY <ul><li>Monitor patients on therapy - Even though the serum bactericidal activity has been associated with a favorable outcome in the treatment of hematogenous osteomyelitis in general, it is not necessary to follow serum bactericidal levels83 because most treatment failures are probably due to a lack of adequate surgical débridement rather than inadequate antibiotic efficacy. </li></ul><ul><li>STAGE 1 </li></ul><ul><li>Stage-1 osteomyelitis in adults is usually treated with antibiotics and operativeintervention. </li></ul><ul><li>appropriate parenteral antimicrobial therapy for four weeks, dated from the initiation of the therapy or from the last major operative débridement </li></ul>Patient responds Arrest Medical management fails Bone & soft tissue debridement & retreat as above
    33. 33. … treatment (cont.) ANTIMICROBIAL THERAPY STAGE 2 In Stage-2 osteomyelitis shorter courses of antibiotics are usually needed Debridement of cortex and soft tissue coverage Appropriate antibiotic for 2 weeks STAGE 3 & 4 Patients with Stage-3 or 4 osteomyelitis are treated with antimicrobial therapy for four to six weeks, dated from the last major débridement. Without adequate débridement, the failure rate is high regardless of the duration of therapy. Even when all necrotic tissue has been adequately débrided, the remaining bed of tissue must be considered contaminated with the responsible pathogen or pathogens. Therefore, it is important to treat the patient with antibiotics for at least four weeks. The arrest rate is about 98% in A hosts and 80% (forStage 4) to 92% (for Stage 3) in B hosts.
    34. 34. Treatment algorithm of Cierny-Mader Stages-3 and 4 long-bone osteomyelitis .
    35. 35. … treatment (cont.) <ul><li>SUPPRESSIVE ANTIBIOTIC THERAPY </li></ul><ul><li>When operative treatment of osteomyelitis is not feasible, suppressive antibiotic therapy, usually administered orally, is usually given to control the disease and to prevent flare-ups. </li></ul><ul><li>Ideal drugs for suppression must possess good bioavailability,have low toxicity, and be able to penetrate bone adequately. </li></ul><ul><li>The suppressive regimen should be directed by the results of cultures. </li></ul><ul><li>Suppressive therapy is traditionally administered for six months. If the infection recurs after discontinuation of the therapy, a new, lifelong suppressive regimen is begun. </li></ul><ul><li>Suppressive therapy for infections around orthopaedic implants has been studied extensively. Rifampin (in combination with other antibiotics), fusidic acid, ofloxacin, and cotrimoxazole have been administered, for six to nine months, to patients with infections around implants. </li></ul>
    36. 36. … treatment (cont.) <ul><li>S U R G I C A L M A N A G E M E N T </li></ul><ul><li>General principles of surgical therapy include </li></ul><ul><li>To remove dead , devitalized and infected bone </li></ul><ul><li>To obliterate any dead space left after debridement </li></ul><ul><li>3. To obtain soft tissue coverage of exposed bone </li></ul><ul><li>Surgery to be undertaken only when – </li></ul><ul><li>1 .Signs and symptoms of acute infection have subsided </li></ul><ul><li>2 . Living bone can be distinguished from dead bone (Sequestra has separated) </li></ul><ul><li>3 .When sufficient involucrum has formed to maintain length and contour of the bone </li></ul>
    37. 37. BONE DEBRIDEMENT <ul><li>The goal of débridement is to leave healthy, viable tissue. </li></ul><ul><li>Débridement of bone is done until punctate bleeding is noted, giving rise to the term the paprika sign . However, even when all necrotic tissue has been adequately débrided, the remaining bed of tissue must still be considered contaminated. </li></ul><ul><li>The extent of operative débridement - B hosts treated with marginal resection (i.e., with a clearance margin of <5 mm) had a higher rate of recurrence than did normal hosts. The extent of resection therefore appears to be much more important in B hosts, whereas a marginal resection may be acceptable in normal hosts. </li></ul>
    38. 38. … Bone Debridement Treatment contd. Procedure ☞ Surgery is done under tourniquet ☞ Infected areas of bone are exposed ☞ Sinus tracts are excised ☞ The periosteum is incised and elevated. Limited elevation of periosteum is done so as to permit a required cortical window at the diseased site. Use of subperiosteal bone levers/ periosteum elevator is undesirable ☞ Cortical window at the appropriate site is marked with a drill and opened with an osteotome
    39. 39. … Bone debridement ☞ All the Sequestra , purulent material ,scarred and necrotic tissue are excised ☞ If sclerotic bone seals the ends of the cavity within the medullary canal , this is opened in both directions. It allows blood vessels to grow into the cavity ☞ Overhanging edges of bone are carefully excised to avoid leaving a cavity or dead space and convert the deep cavity into a superficial saucer like cavity ☞ Tourniquet is removed so as to see oozing bone all around ☞ Sclerosed ,nonviable bone if any is also removed
    40. 40. … Bone Debridement <ul><li>There are few sites where radical excision can easily be done by excision of a segment of whole bone and radical excision does not have any residual appreciable functional or cosmetic defect </li></ul><ul><li>Such sites are : </li></ul><ul><li>upper 3/4th of fibula </li></ul><ul><li>ribs </li></ul><ul><li>clavicle </li></ul><ul><li>Metacarpals/metatarsals </li></ul><ul><li>tarsal bones </li></ul><ul><li>scapula </li></ul>
    41. 41. Obliteration of dead space: Adequate debridement often leaves a large dead space that must be managed to prevent recurrence and significant bone loss that may result in bony instability. Appropriate reconstruction of both the bones and soft tissue defect may be needed
    42. 42. .) Various methods to obliterate the dead space so left are ☞ surrounding soft tissue ☞ local muscle flap ☞ vascularized muscle pedicle flap ☞ microvascular free tissue transfer which may be of three types . osseous free flaps . osteocutaneous free flaps . myocutaneous free flaps ☞ Autogenous cancellous bone graft ☞ PMMA antibiotic bead chain ☞ Biodegradable substances impregnated with antibiotics ☞ free fibular grafts ☞ bone transport by Ilizarov
    43. 43. .) Soft tissue coverage  . Primary wound closure  . If the soft tissue conditions do not permit primary closure, the most favoured and acceptable method consist of delayed closure after 4-7 days, when the wound looks healthy ,and there is no collection of purulent material at the depth of wound . The success of such secondary closure depends on 1 rapid and complete conrol of subjacent bone infection 2 presence of healthy vascular granulating surfaces on the sides and depth of wound and 3 anatomical configuration of the wound which permits the wound surfaces to be brought together without excessive tension
    44. 44. .) <ul><li>When secondary closure is not possible options available to the surgeon are </li></ul><ul><li>1 Initial split thickness graft so as to obtain complete closure of the wound : The disadvantage of this procedure is that it leaves an unstable scar specially if grafts are placed on exposed bone but such scars mature in course of time . The advantages are : It is simple ,safe and can be done by any surgeon . As such, wherever feasible ,it is most commonly employed method </li></ul><ul><li>2 Where collaboration with a plastic surgeon colleague is available and the patient can afford prolonged and expensive treatment ,following options are available </li></ul><ul><ul><li>1.Full thickness rotation flaps </li></ul></ul><ul><ul><li>2. Cross limb flaps </li></ul></ul><ul><ul><li>3.Free flap </li></ul></ul><ul><ul><li>4. Muscle pedicle graft </li></ul></ul><ul><ul><li>5. Bone graft to fill up bone cavities combined with subsequent full thickness </li></ul></ul><ul><ul><li>skin flaps </li></ul></ul><ul><ul><li>6.Use of Ilizarov techniques where major gaps are left in a bone and bone </li></ul></ul><ul><ul><li>transport is required to fill bone gap </li></ul></ul>
    45. 45. All the three objectives can be achieved as: <ul><li>A single stage procedure </li></ul><ul><li>Two Stage procedure- The Belfast Technique (McNally et al) </li></ul><ul><li>Three Stage Procedure- The Pappineau’s Technique </li></ul>
    46. 46. The Belfast Techinque <ul><li>Two stage procedure </li></ul><ul><li>Radical debridment </li></ul><ul><li>Delayed autogenous bone grafting when necessary </li></ul>
    47. 47. <ul><li>Pappineau’s method : </li></ul><ul><li>This is a three stage operation : </li></ul><ul><li>Excision of infected tissue with or without stabilization( external fixator/intramedullary nail </li></ul><ul><li>Autogenous cancellous bone graft </li></ul><ul><li>Skin closure </li></ul>
    48. 48. chronic osteomyelitis(contd.) <ul><li>Treatment contd </li></ul><ul><li>Principles( Pappineau’s technique) </li></ul><ul><li>Granulation tissue markedly resists infection </li></ul><ul><li>Autogenous cancellous bone graft are resistant to </li></ul><ul><li>infection and are rapidly revascularized </li></ul><ul><li>Infected area is completely excised </li></ul><ul><li>Adequate drainage is provided </li></ul><ul><li>Adequate stabilization is provided </li></ul><ul><li>Antibiotics are used for prolonged period </li></ul>
    49. 49. .) Pappineau’s method continued Stage 1 : Radical debridement with or without stabilization and pack the wound open with dressings soaked in antibiotics . First dressing after 4 to 5 days then daily .Excise infected tissue as necessary and delay second stage till signs of infection have disappeared and healthy granulation tissue is present throughout Stage 2 : Bone grafting … strips of autogenous cancellous bone are packed in concentric and overlapping layers till cavity is overfull . Again pack the wound open with dressing soaked in antibiotic . First dressing between 3rd to 5th day . Replace any graft that adheres to dressing. Continue dressing until the graft stabilize. Muscle pedicle graft to enhance the blood supply may also be done along with . Stage 3 : Wound coverage : if spontaneous epithelisation do not provide adequate wound coverage this can be provided by secondary wound closure ,skin grafts, myocutaneous flaps , muscle pedicle flaps and free flaps
    50. 50. .) PMMA Antibiotic bead chain technique :: The rationale for this treatment is to deliver levels of antibiotics locally in concentrations that exhibit the minimal inhibitory concentrations .Local concentrations of antibiotic achieved are up to 200 times higher than levels achieved with systemic administration. This has the advantage of obtaining very high local antibiotic concentrations while maintaining low serum levels and low systemic toxicity High concentration of antibiotic can be achieved only with primary wound closure ;if such closure cannot be performed, the wound can be covered with a water impermeable dressing (bead pouch technique)
    51. 51. .) Biodegradable antibiotic delivery system (Osteoset Reabsorbable Bead kit,Wright Med. Technologies) Various biodegradable antibiotic system have been evaluated . The advantage of these is, that a second procedure to remove the implants is not required . Furthermore these substances act as an osteoconductive bone graft substitute as well as deliver antibiotics locally like PMMA beads and gets reabsorbed in about 8 weeks after surgery
    52. 52. .) Closed suction drainage .. To deliver antibiotic locally at higher concentration ,Surgeons ( Hashmi et al ),have recommended closed irrigation by antibiotic solution and continuous suction of irrigated fluid . However secondary contamination and infection with new organism may occur and therefore most surgeons have abandoned this method
    53. 53. Hyperbaric Oxygen therapy Hyperbaric oxygen therapy has been recommended for treatment of chronic osteomyelitis but has not proved to be effective in isolation .It can be used as adjuvant to traditional methods of treatment
    54. 54. .) <ul><li>Amputation . </li></ul><ul><li>is reserved only for those extreme cases of chronic osteomyelitis where: </li></ul><ul><ul><ul><li>persistence of severe pus pouring infection of very long duration , not responding to multiple operative interventions </li></ul></ul></ul><ul><ul><ul><li>2 . systemic complication like amyloidosis / CRF </li></ul></ul></ul><ul><ul><ul><li>3 . infection associated with extensive deformation of neighboring joints and low socioeconomic status of the patient / high risk patients who cannot afford / tolerate multiple surgeries </li></ul></ul></ul><ul><ul><ul><li>4 . chronic osteomyelitis associated with vascular complications </li></ul></ul></ul><ul><ul><ul><li>5 . chronic osteomyelitis with epithelioma </li></ul></ul></ul>
    55. 55. INFECTED IMPLANTS <ul><li>The absolute number of patients with implant-associated infections is on the rise due to the lifelong risk for bacterial seeding on the implant. </li></ul><ul><li>Infections associated with prosthetic joints occur less frequently than aseptic failures, but represent the most devastating complication with high morbidity and substantial cost . </li></ul><ul><li>In patients with primary hip replacement, the infection rate during the first 2 years is usually less than 1%, and in those with knee replacement less than 2%. </li></ul><ul><li>Infection rates after revision surgery are usually considerably higher (40%) than after primary replacement </li></ul><ul><li>About 5% of internal fixation devices become infected . The incidence of infection after internal fixation of closed fractures is generally lower (2%), whereas the incidence may exceed 30% after fixation of open fractures </li></ul>
    56. 56. INFECTED IMPLANTS <ul><li>The pathogenesis of implant-associated infection involves interaction between microorganisms, the implant and the host </li></ul><ul><li>The foreign implant is both a predisposing factor and an important element in its persistence. </li></ul><ul><li>Bacteria as well as human tissue cells have an affinity for the molecules on the surface of implant. Both compete for occupancy on the same surface – tissue cells by adaptation and integration; bacteria by adhesion and colonization. This contest has been aptly called the race for the surface. If the tissue cells win, implant is incorporated, if bacteria win the resultant infection usually persists until the implant is removed. </li></ul><ul><li>Implant-associated infections are typically caused by microorganisms growing in structures, known as biofilms . As orthopaedic implants and materials are increasingly moving towards minimizing the immune response they are becoming more and more inert and hence susceptible to bacterial adhesion and colonization, </li></ul>
    57. 57. CLASSIFICATION OF PERIPROSTHETIC INFECTIONS <ul><li>Positive Intraoperative Cultures – Two or more positive cultures from the surgical site. </li></ul><ul><ul><li>Treatment - appropriate parentral antibiotics for 6 weeks </li></ul></ul><ul><ul><li>Early Postoperative Infection – Infection occurs within first month after arthroplasty. Clinically apparent wound infections or infections of hematomas that have progressed to deep infections </li></ul></ul><ul><ul><li>Treatment - debridement, exchange of the polyethylene liners, retention of the components, and intravenous administration of antibiotics for 4 weeks. </li></ul></ul><ul><li>Late Chronic Infection - infection is apparent more than 1 month after the operation and has an insidious clinical onset . Typically, patients have never had a pain-free interval after the operation </li></ul><ul><li>Treatment - debridement, removal of the components, and appropriate antibiotics for 4 to 6 weeks. This may be followed by implantation of a new prosthesis after the patient has been free of infection. </li></ul><ul><li>4. Acute Hematogenous Infection - The acute infection is characterized by the precipitous onset of clinical symptoms in a previously well-functioning hip. </li></ul><ul><li>Treatment - If the prosthesis is well fixed, treat the infection in the same manner as for an early postoperative infection; if the prosthesis is loose, treatment should be the same as for a late chronic infection. </li></ul>
    58. 58. Infections in internal fixation devices <ul><li>A patient with an infected internal fixation device usually has increasing or new onset of pain that may be located at the implant insertion site or at the fracture site. The pain is often described as dull and deep within the extremity and exacerbated by activity. </li></ul><ul><li>Local signs may include cellulitis, abscess formation, and wound drainage. </li></ul><ul><li>Constitutional symptoms include fever, chills, night sweats, tachycardia, and anemia. </li></ul><ul><li>Past medical history may reveal risk factors such as cigarette smoking, diabetes, alcohol abuse, previous open fracture, or previously draining wound </li></ul><ul><li>Several recent studies have shown a high infection rate in patients undergoing delayed intramedullary fixation following external fixation, particularly if there has been an infected pin site . </li></ul>
    59. 59. <ul><li>The method of treatment of infection after internal fixation is based upon: </li></ul><ul><li>The time of onset after internal fixation (Early/Late) </li></ul><ul><li>The status of fracture healing. </li></ul><ul><li>The stability of the implants and fracture. </li></ul><ul><li>The extent of radiographic bone involvement. </li></ul><ul><li>The type and virulence of the organism. </li></ul><ul><li>The patients general condition and health </li></ul><ul><li>Obtain radiographs as soon as the diagnosis is suspected to assess the stability of the fixation construct. Radiolucency around the fixation devices suggests loose hardware. Assess fracture healing as well. Do not confuse periosteal reaction from the infection with fracture callus Plain tomography may assist in the assessment of fracture healing. Finally, classic signs of osteomyelitis with involucrum or sequestrum may be present </li></ul>
    60. 62. a 46-year-old man with chronic osteomyelitis. The patient was treated with debridement followed by insertion of aminoglycoside-impregnated methylmethacrylate beads and a local muscle flap.
    61. 63. THANK YOU