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Premium member Presentation Transcript OSTEOMYELITIS: OSTEOMYELITIS Dr N aseel SalimSlide 2: The term osteomyelitis literally means inflammation of bone and its marrow Now it is commonly used for infectionSlide 3: In New borns - S. aureus , , and group B Streptococcus In Children (up to 4 y) - S. aureus , group B Streptococcus species , and Haemophilus influenzae , In Children, adolescents (aged 4 y to adult) - S.aureus (80%), group A Streptococcus species, H. influenzae , In Adult - S. aureus and Coagulase-negative Staphylococcus species occasionally Enterobacter or Streptococcus species P aeruginosa ( iv drug abusers ) E coli ,Pseudomonas , Klebsiella spp -patients with UTI In Sickle Cell Anaemia Patients - Salmonella species Fungus also causes osteomyelitis. Etiological agents:Slide 4: - S. aureus RESPONSIBLE FOR 80-90% OSTEOMYELITISPathogenesis: Pathogenesis Hematogenous -common in children Direct inoculation (usually traumatic or surgical) Local invasion from a contiguous infection (usually decubitus ulcer or periodontal disease)Slide 6: Hematogenous osteomyelitis highest in children < 5 years of age. In adult- Haematogenous is less common but if they suffered due to debility,disease (diabetes mellitus)drugs( immunosuppresion ).Slide 7: Metaphysis of long bones Anatomy Non anastomosing end artery with sharp loops Slow and turbulent blood flow Metaphyseal capillaries--- lack phagocytic lining cellspathogenesis: pathogenesisSlide 9: Trauma or emboli lead to occlusion of the slow-flowing sinusoidal vessels, further establishing a nidus for infection. Once localised in the bone the bacteria proliferate and cause cell death The entrapped bone undergo necrosis with in 48 hours The bacteria and inflammation spread through shaft of bone And may percolate through haversian system to reach the periosteumSlide 10: Pus spreads into the bone's blood vessels, impairing their flow, and areas of devitalized infected bone, known as SEQUESTRA , Often, the body will try to create new bone around the area of necrosis. The resulting new bone is often called an INVOLUCRUM. Histologic examination, these areas of necrotic bone are the basis for distinguishing between acute and chronic osteomyelitis. Soft tissue abscess and draining sinusFactors That Turn Acute Bone Infection to Chronic Osteomyelitis:: Factors That Turn Acute Bone Infection to Chronic Osteomyelitis : Trauma (orthopaedic surgery or open fracture) Prosthetic orthopaedic device Diabetes Peripheral vascular disease Chronic joint disease Alcoholism Intravenous drug abuse Chronic steroid use Immunosuppression Tuberculosis HIV and AIDS Sickle cell disease Presence of catheter-related blood stream infection.Direct inoculation : Direct inoculation TRAUMA PERIOPERATIVE INTRAOPERATIVE INTERNAL FIXATION PROSTHESIS OPEN FRACTURE CHRONIC SOFT TiSSUE INFECTIONSlide 13: MULTIPLE ORGANISMS CAN BE ISOLATED MOST COMMON S. aureus Local invasion from a contiguous infection : Local invasion from a contiguous infection Diabetes Peripheral vascular disease Chronic joint disease SMALL BONES OF FEET MOSTLY AFFECTED MULTIPLE ORGANISMS ISOLATED Coagulase +VE /-VE Staphylococcus Streptococcus species Enterococcus spp GNB AnaerobesClassification of Osteomyelitis: Classification of Osteomyelitis Duration of infection Acute ( <2 WEEKS) Sub acute (2-3 WEEKS) Chronic ( >3 WEEKS)Symptoms( acute) : Symptoms( acute) Fever>102ºF pain in the infected bone. The area over the bone may be sore, warm, and swollen, and movement may be painful. The person may lose weight and feel tired.Symptoms (chronic ): Symptoms (chronic ) Chronic pain Discharge Fever(low grade )Chronic osteomyelitis : Chronic osteomyelitis Local bone loss Persistent drainage Sinus tractVertebral osteomyelitis : Vertebral osteomyelitis usually hematogenous in origin but may be secondary to trauma causing persistent back pain and tenderness . Pain worsens with movement and N ot relieved by resting, applying heat, or taking analgesics. Fever is often absent.Laboratory findings: Laboratory findings Elevations in the peripheral white blood cell count ( WBC ) Erythrocyte sedimentation rate ( ESR ), and C-reactive protein ( CRP ) in children -are variable and nonspecific but elevated in adults Blood culture is positive in half of cases Culture of bone biopsy is needed to identify the specific pathogen A lternative are needle puncture or surface swabs are easier to perform, but do not produce reliable results. In almost 50% cases no organisms isolatedImaging studies: Imaging studies X ray : soft tissue swelling Periosteal thickening /elevation focal osteopenia Radiographic evidence of bone destruction finally becomes apparent by 10 to 21 days.Slide 23: Magnetic resonance imaging (MRI) Modality of choice Accurate identification of subperiosteal or soft tissue collections of pus. no radiation. Excellent anatomic detail and differentiation among soft tissue, bone marrow, and boneScintigraphy: Scintigraphy Radio nucleotide TC 99m Poly Phosphate scan Gallium citrate scan Indium Sensitivity (84 to 100 percent) and specific (70 to 96 percent)Computed tomography : Computed tomography Planning the surgical approach to debridement of sequestra Evaluating the patient being treated for osteomyelitisManagement And Treatment : Management And Treatment Early clinical suspicion, confirmation through imaging and microbiological tests and prompt treatment are the keys to a successful outcomeSlide 27: In acute osteomyelitis- The principle of treatment are- 1.General supportive treatment Analgesic for relieve pain I/V fluid(fever with shock, septicaemia) 2.Splintage of the affected part 3.Antibiotics(oral/intravenous)-It should be started immediately not waiting for culture of blood and pusTreatment : Treatment Antimicrobials Debridement surgery Dead space management Stabilisation ReconstructionAcute heametogenous : Acute heametogenous Primarily a medical disease The infection is susceptible to definitive antimicrobials If not responding within 48 hrs. , surgical approach needed A bone biopsy for culture is necessary after that only antibiotics started The antibiotics continued or changed according to the culture results Antibiotics are given for 4-6 weeksVertibral osteomyelitis: Vertibral osteomyelitis Bone biopsy Blood culture –usually sterile 4-6 weeks antibioticsc/c osteomyelitis : c/c osteomyelitis Adequate drainage Thorough debridement Obliteration of dead space wound infection Antimicrobial therapySlide 32: Methicillin sensitive : clindamycin MRSA :PENICILLIN –RIFAMPICIN VANCOMYCIN –RIFAMPICIN Antibiotic (Gentamycin ) impregnated acrylic beads removed within 2-4 weeks ,and replaced with cancellous bone graft Antibiotic ( clindamycin,amikacin )delivered directly into dead space with an implantable pumpSlide 34: Stability Plates ,screws ,rods , or external fixation Ilizarovs external fixator Objectives of surgery- Drain any abscess cavity Remove all non viable tissue Operation-procedures are : 1.Saucharization and curettage 3. muscle flap transferComplications of acute osteomyelitis : Complications of acute osteomyelitis Bone abscess Septic Arthritis Bacteraemia Fracture Growth arrest Loosening of the prosthetic implant Overlying soft-tissue cellulitis Chronic infectionPrognosis: Prognosis This is variable depending on the number of risk factors and the patient's general condition Outcome is best if treatment is started 3-5 days after onset of the infection. Timely diagnosis and intervention in an otherwise well patient should lead to full recovery, although follow-up over several months will be required to monitor for relapse.Other clinical situations : Other clinical situations Heamodialysis -S. aureus and S.epidermidis Sickle cell disease – GNB ,Salmonella spp Heroin addicts -S. aureus and S.epidermidis ,GNB, candida spp Brodies abscess -c/c localised bone abscess: Skeletal tuberculosis Non tubercular mycobacteria M. marinum M. avium intracellulare M fortuvitum M chelonae M ulcerans M kansasiFungal osteomyelitis : Fungal osteomyelitis Coccidiodomycosis Blastomycosis C ryptococcosis C andidiasis Sporotrichosis Treatment surgical debridement and antifungal chemotherapy You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
OSTEOMYELITIS MY drnaseelsalim Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 219 Category: Entertainment License: All Rights Reserved Like it (0) Dislike it (0) Added: March 26, 2011 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript OSTEOMYELITIS: OSTEOMYELITIS Dr N aseel SalimSlide 2: The term osteomyelitis literally means inflammation of bone and its marrow Now it is commonly used for infectionSlide 3: In New borns - S. aureus , , and group B Streptococcus In Children (up to 4 y) - S. aureus , group B Streptococcus species , and Haemophilus influenzae , In Children, adolescents (aged 4 y to adult) - S.aureus (80%), group A Streptococcus species, H. influenzae , In Adult - S. aureus and Coagulase-negative Staphylococcus species occasionally Enterobacter or Streptococcus species P aeruginosa ( iv drug abusers ) E coli ,Pseudomonas , Klebsiella spp -patients with UTI In Sickle Cell Anaemia Patients - Salmonella species Fungus also causes osteomyelitis. Etiological agents:Slide 4: - S. aureus RESPONSIBLE FOR 80-90% OSTEOMYELITISPathogenesis: Pathogenesis Hematogenous -common in children Direct inoculation (usually traumatic or surgical) Local invasion from a contiguous infection (usually decubitus ulcer or periodontal disease)Slide 6: Hematogenous osteomyelitis highest in children < 5 years of age. In adult- Haematogenous is less common but if they suffered due to debility,disease (diabetes mellitus)drugs( immunosuppresion ).Slide 7: Metaphysis of long bones Anatomy Non anastomosing end artery with sharp loops Slow and turbulent blood flow Metaphyseal capillaries--- lack phagocytic lining cellspathogenesis: pathogenesisSlide 9: Trauma or emboli lead to occlusion of the slow-flowing sinusoidal vessels, further establishing a nidus for infection. Once localised in the bone the bacteria proliferate and cause cell death The entrapped bone undergo necrosis with in 48 hours The bacteria and inflammation spread through shaft of bone And may percolate through haversian system to reach the periosteumSlide 10: Pus spreads into the bone's blood vessels, impairing their flow, and areas of devitalized infected bone, known as SEQUESTRA , Often, the body will try to create new bone around the area of necrosis. The resulting new bone is often called an INVOLUCRUM. Histologic examination, these areas of necrotic bone are the basis for distinguishing between acute and chronic osteomyelitis. Soft tissue abscess and draining sinusFactors That Turn Acute Bone Infection to Chronic Osteomyelitis:: Factors That Turn Acute Bone Infection to Chronic Osteomyelitis : Trauma (orthopaedic surgery or open fracture) Prosthetic orthopaedic device Diabetes Peripheral vascular disease Chronic joint disease Alcoholism Intravenous drug abuse Chronic steroid use Immunosuppression Tuberculosis HIV and AIDS Sickle cell disease Presence of catheter-related blood stream infection.Direct inoculation : Direct inoculation TRAUMA PERIOPERATIVE INTRAOPERATIVE INTERNAL FIXATION PROSTHESIS OPEN FRACTURE CHRONIC SOFT TiSSUE INFECTIONSlide 13: MULTIPLE ORGANISMS CAN BE ISOLATED MOST COMMON S. aureus Local invasion from a contiguous infection : Local invasion from a contiguous infection Diabetes Peripheral vascular disease Chronic joint disease SMALL BONES OF FEET MOSTLY AFFECTED MULTIPLE ORGANISMS ISOLATED Coagulase +VE /-VE Staphylococcus Streptococcus species Enterococcus spp GNB AnaerobesClassification of Osteomyelitis: Classification of Osteomyelitis Duration of infection Acute ( <2 WEEKS) Sub acute (2-3 WEEKS) Chronic ( >3 WEEKS)Symptoms( acute) : Symptoms( acute) Fever>102ºF pain in the infected bone. The area over the bone may be sore, warm, and swollen, and movement may be painful. The person may lose weight and feel tired.Symptoms (chronic ): Symptoms (chronic ) Chronic pain Discharge Fever(low grade )Chronic osteomyelitis : Chronic osteomyelitis Local bone loss Persistent drainage Sinus tractVertebral osteomyelitis : Vertebral osteomyelitis usually hematogenous in origin but may be secondary to trauma causing persistent back pain and tenderness . Pain worsens with movement and N ot relieved by resting, applying heat, or taking analgesics. Fever is often absent.Laboratory findings: Laboratory findings Elevations in the peripheral white blood cell count ( WBC ) Erythrocyte sedimentation rate ( ESR ), and C-reactive protein ( CRP ) in children -are variable and nonspecific but elevated in adults Blood culture is positive in half of cases Culture of bone biopsy is needed to identify the specific pathogen A lternative are needle puncture or surface swabs are easier to perform, but do not produce reliable results. In almost 50% cases no organisms isolatedImaging studies: Imaging studies X ray : soft tissue swelling Periosteal thickening /elevation focal osteopenia Radiographic evidence of bone destruction finally becomes apparent by 10 to 21 days.Slide 23: Magnetic resonance imaging (MRI) Modality of choice Accurate identification of subperiosteal or soft tissue collections of pus. no radiation. Excellent anatomic detail and differentiation among soft tissue, bone marrow, and boneScintigraphy: Scintigraphy Radio nucleotide TC 99m Poly Phosphate scan Gallium citrate scan Indium Sensitivity (84 to 100 percent) and specific (70 to 96 percent)Computed tomography : Computed tomography Planning the surgical approach to debridement of sequestra Evaluating the patient being treated for osteomyelitisManagement And Treatment : Management And Treatment Early clinical suspicion, confirmation through imaging and microbiological tests and prompt treatment are the keys to a successful outcomeSlide 27: In acute osteomyelitis- The principle of treatment are- 1.General supportive treatment Analgesic for relieve pain I/V fluid(fever with shock, septicaemia) 2.Splintage of the affected part 3.Antibiotics(oral/intravenous)-It should be started immediately not waiting for culture of blood and pusTreatment : Treatment Antimicrobials Debridement surgery Dead space management Stabilisation ReconstructionAcute heametogenous : Acute heametogenous Primarily a medical disease The infection is susceptible to definitive antimicrobials If not responding within 48 hrs. , surgical approach needed A bone biopsy for culture is necessary after that only antibiotics started The antibiotics continued or changed according to the culture results Antibiotics are given for 4-6 weeksVertibral osteomyelitis: Vertibral osteomyelitis Bone biopsy Blood culture –usually sterile 4-6 weeks antibioticsc/c osteomyelitis : c/c osteomyelitis Adequate drainage Thorough debridement Obliteration of dead space wound infection Antimicrobial therapySlide 32: Methicillin sensitive : clindamycin MRSA :PENICILLIN –RIFAMPICIN VANCOMYCIN –RIFAMPICIN Antibiotic (Gentamycin ) impregnated acrylic beads removed within 2-4 weeks ,and replaced with cancellous bone graft Antibiotic ( clindamycin,amikacin )delivered directly into dead space with an implantable pumpSlide 34: Stability Plates ,screws ,rods , or external fixation Ilizarovs external fixator Objectives of surgery- Drain any abscess cavity Remove all non viable tissue Operation-procedures are : 1.Saucharization and curettage 3. muscle flap transferComplications of acute osteomyelitis : Complications of acute osteomyelitis Bone abscess Septic Arthritis Bacteraemia Fracture Growth arrest Loosening of the prosthetic implant Overlying soft-tissue cellulitis Chronic infectionPrognosis: Prognosis This is variable depending on the number of risk factors and the patient's general condition Outcome is best if treatment is started 3-5 days after onset of the infection. Timely diagnosis and intervention in an otherwise well patient should lead to full recovery, although follow-up over several months will be required to monitor for relapse.Other clinical situations : Other clinical situations Heamodialysis -S. aureus and S.epidermidis Sickle cell disease – GNB ,Salmonella spp Heroin addicts -S. aureus and S.epidermidis ,GNB, candida spp Brodies abscess -c/c localised bone abscess: Skeletal tuberculosis Non tubercular mycobacteria M. marinum M. avium intracellulare M fortuvitum M chelonae M ulcerans M kansasiFungal osteomyelitis : Fungal osteomyelitis Coccidiodomycosis Blastomycosis C ryptococcosis C andidiasis Sporotrichosis Treatment surgical debridement and antifungal chemotherapy