Acute and Chronic Osteomyelitis - Infection of BoneRahul Singh
Acute and Chronic Osteomyelitis - Infection of Bone
http://essentialinspiration4u.blogspot.com
Osteomyelitis is defined as an acute or chronic inflammatory process of bone, bone marrow and its structure secondary to infection with micro organisms.
Duration , Mechanism & Host response.
Duration - Acute / Subacute / Chronic
Mechanism - Heamatogenous (tonsil , lungs , ear/ GIT) - Exogenous (injection , open fractures)
Host response - Pyogenic / Granulomatous
Introduction of bacteria from :
Outside through a wound or continuity from a neighboring soft tissue infection
Hematogenous spread from a pre existing focus (most common route of infection)
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Imaging features of acute and chronic osteomyelitis are described in this PPT. Infective arthritis along with fungal infections of soft tissue are also covered very well. Special emphasis is given on tubercular infection of bone.
Highly malignant tumor of mesenchymal origin.Spindle shaped cells that produce osteoid.2nd most common primary malignant bone tumor after MM.Incidence – 1 to 3 per million per year
Treated by chemo,amputation or rotationplasty
Osteomyelitis is an infection in a bone. Infections can reach a bone by traveling through the bloodstream or spreading from nearby tissue. Infections can also begin in the bone itself if an injury exposes the bone to germs.
Smokers and people with chronic health conditions, such as diabetes or kidney failure, are more at risk of developing osteomyelitis. People who have diabetes may develop osteomyelitis in their feet if they have foot ulcers.
Although once considered incurable, osteomyelitis can now be successfully treated. Most people need surgery to remove areas of the bone that have died. After surgery, strong intravenous antibiotics are typically needed.
Osteomyelitis may be a very dreadful condition for both the suffering patient & the treating orthopaedic surgeon.Here is the brief presentation on it deeply focused on its standard management.
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the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
8. Pathological Features Hallmark is bone necrosis Exudation of PMNL, large no. of lymphocytes, histiocytes and plasma cells( occasionally ) Formation of new bone (involucrum) from surviving periosteum & endosteum Involucrum- enveloping sheet of live bone with perforations (cloacae) for pus to drain to the exterior causing chronic sinus
9. Proliferation of endosteal new bone causing obliteration of medullary canal Prostaglandin E production is increased many folds in infected bone causing bone resorption & sequestration formation Resorption is mediated by several cytokines –IL-1, IL-6, IL-11 & TNF α
10. Why Chronicity ? Negative charge on surface of devitalized bone promotes organism adherence and subsequent glycocalyx formation thereby preventing access to phagocytes & microbials. Bacteria enter the interior of the cell eluding host defense. Dead & dying osteoblast release viable S. Aureus causing persistence of infection & its flare up.
11. Main infecting organism is likely to be the same organism as when present at the original attack even if a recurrent episode occurs years later!! Sharrad .pediatric orthopedics & fractures vol-II
12. Labs Leukocyte count- in acute OM, often normal in chronic cases (elevated in only 35%) ESR– in both . after T/t- but increases immediately after operative debridement. Not a sensitive test to r/o acute or chronic OM, not reliable in compromised host/isolated findings ± CRP - in acute/chronic, faster than ESR, more sensitive. Favorable outcome if CRP decreases within 3 days of antibiotic treatment in acute cases, test weekly in acute & every ? 2 wks in chronic OM
13. Monitoring drug toxicity Serum creatinine levels Liver function tests Nutritional status S. albumin level Total iron binding capacity Blood culture- yield approx. 60% PCR Culture & sensitivity- discharge/sinus Deep bone biopsy- yield approx. 90% ( gold standard)
14. Microbiology Bone culture/deep bone biopsy are a must except in Cierny-Mader stage-1 where blood/ joint fluid cultures obviate need of biopsy Culture of samples from sinus tract is not reliable for predicting which organism will be isolated from infected bone
15. Comparision of results of bacterial cultures from multiple sites in chronic OM Patzakis et al JBJS, 1994;76A:664-666 Culture from sinus tract , purulent fluid, soft tissue & bone for aerobic /anaerobic/ fungal growth yielded organisms- >1 in 21/30 >3 in 11/30 10 in 2/30 Same org. in 14/30( only in 47% ) Recommendation is to send all 4 specimens –to identify as many organisms as possible. +ve co-relation has been found between S. aureus growth from sinus tract & that from bone culture.
17. CT Scan To identify areas of necrotic bone/ sequestra Help in establishing a surgical plan MRI High sensitivity & specificity for diagnosis Localises abnormal bone marrow early Can detect myositis, cellulitis, sinus tract formation & soft tissue abscess “Rim sign”-in chronic OM is high signal intensity surrounding the focus of active disease
18. Radionuclide scan Used when diagnosis is ambiguous Gauges extent of bone & soft tissue inflammation -99mTc - 67 Gallium citrate - 111 Indium labelled leukocytes-ideally for acute OM. MRI-is much more sensitive than nuclear studies . During the 1st post-op year MRI can not accurately distinguish infection from fibrovascular scar—COMBINEDNUCLEAR MEDICINE STUDIES WERE FOUND TO BE MORE USEFUL DURING THIS PERIOD
19. 18FDG PET Scan Meta-analysis showed –Fluorodeoxyglucose positron emission tomography has the highest accuracy for confirming or excluding the diagnosis of Chr OM “The Accuracy of Diagnostic Imaging for the Assessment of ChronicOsteomyelitis: A Systematic Review and Meta-Analysis” The Journal of Bone and Joint Surgery (American). 2005;87:2464-2471.
21. Radiologic Classification of Chronic Hematogenous Osteomyelitis in Children Henry Wynn Jones, FRCS (T&O), James W. Harrison, FRCS (T&O), Jeremy Bates, FCS (ECSA), Gwyn A. Evans, FRCS, and Nicolas Lubega, FCS (ECSA) J Pediatr Orthop Volume 29, Number 7, October/November 2009 Chronic Hematogenous Osteomyelitis in Children
22. Classification Type A—Brodie’s abscess, Type B—Sequestrum involucrum, B1-Localised cortical sequestrum B2-Sequestrum with normal /structural involucrum* B3-Sequestrum with sclerotic involucrum B4-Sequestrum without structural involucrum Type C—sclerotic. If proximal physis is damaged the suffix P is added If distal physis is affected the suffix D is added * Adequate involucrum to support wt of limb against gravity
23. Beit CURE Classification of Childhood Haematogenous Chronic Osteomyelitis Example of type C: sclerotic tibia. Example of type A: Brodie’s abscess within a distal tibia
24. Beit CURE Classification of Childhood Haematogenous Chronic Osteomyelitis Example of type B1:localised cortical sequestrum of a tibia. Example of type B2: sequestrum with normal structural involucrum of a proximal humerus.
25. Beit CURE Classification of Childhood Haematogenous Chronic Osteomyelitis Example of type B4: sequestrum with structurally inadequate involucrum of a tibia. Example of type B3: sequestrum with sclerotic involucrum of a radius.
26. TREATMENT MEDICAL Specific antimicrobial coverage In compromised host—correct or reduce the host defect SURGICAL Adequate drainage Debridement Obliteration of dead space Adequate soft tissue cover for wound protection Restoration of an effective blood supply
27. ANTIBIOTIC TREATMENT Chronic infection develops in 19% of pt with acute osteomyelities receiving antibiotics for 3 wks or less---BUT only 2% in patients receiving longer than 3 wks Cierny-Mader stage 1,3,4 require 4 - 6 wks of antibiotics (revascularisation of bone after debridement takes about 4 wks) Stage 2—short course antibiotics for 2 wks following debridement of cortex/soft tissue Stage 3 /4 –antibiotics for 4 to 6 wks from last major decompression/debridement
28. ANTIBIOTICS IV antibiotics Nafcillin/oxacillin/nafcillin with rifampcin * Vancomycin/ampcillin/cefazolin/ceftriaxone Clindamycin/sulbactum/piperacillin/tazobactam ORAL antibiotics Clindamycin/rifampcin/cotrimexazole Fluroquinolones in gram –ve organisms Linezolid-oral & IV antibiotics—MRSA
29. Not necessary to follow serum bactericidal levels-failure are due to lack of adequate surgical debridement rather than inadequate antibiotic efficiency In children the benefits of Quinolones if required are much more than toxicity to joint which is rare except in cystic fibrosis Ball p et all drug safe 1999;21:407-21
30. Out Patient Parentral Antibiotic Therapy OPAT 51% courses associated with ADE(adverse drug event) 32.5% of antibiotics were discontinued because of ADE Vancomycin has highest ADE rate (85.7%) Ceftrixone has highest discontinuation rate of 66.7% Cefazolin had the lowest rate of ADE & ADE related discontinuation rate at 0% for both Leukopenia/hepatitis/rash (Paediatric Infectious disease journal ,july 2009)
31. OPERATIVE TREATMENT Bone debridement Complete removal of all infective / devascularized tissue –only solution to eradicate infection—a/b cannot reach “Paprika sign” –punctate bleeding Extent of operative debridement- (simpson et all) >5 mm wide resection-no recurrence <5 mm marginal resection had recurrence of 28% Extent of debridement is much more important in B hosts Cortical window- at weakest area of the involucrum -connect a series of drill holes -should be oval to mimimise risk of # IF INITIAL DEBRIDMENT IS IN DOUBT RETURN TO OT FOR ADDITIONAL DEBRIDEMENT
32. When to do sequestrectomy? Early sequestrectomy - Eradicate infection - Better environment for periosteum to respond Delayed sequestrectomy Wait till sufficient involucrum has formed before doing a sequestrectomy to mimimize the risk of cx, fracture, deformity & segmental loss In either case it is critical to preserve the involucrum preferable to wait at least 3-6 mo before performing a sequestrectomy
34. Post sequestrectomy NO STABLISATION IS NECESSARY WHEN 70% OF THE ORIGINAL CORTEX REMAINS INTACT If >70% cortical volume has been retained—protect by cast Greater bone loss-Ext fix Focal bone loss-open cancellous BG/conventional BG Seg. bone loss—BG/Bone transport/other devices Radiologically if cortical continuity of the involucrum is 50% of the over all cortical diameter on 2 orthogonal views then the involucrum is structurally adequate
35. The sequestrum here is a large segment of the tibial diaphysis, and a suitable involucrum had formed posteriorly and laterally . At the time of exposure, that segment was avascular in contrast to the surrounding bone and soft tissue. The segment was easily removed.
36. The failure to form an adequate involucrum will result in segmental bone loss.
40. Treatment algorithm of Cierny-Mader Stages-3 and 4 long-bone osteomyelitis. Osteomyelitis in long bones, L . Lazzarini,J.T.Mader,JBJS.Am.2004;86:2305-2318
41. Chronic OM with segmental bone loss Either partial or entire Forearm/lower limb-by pass procedures may be used to restore stability—HUNTINGTON PROCEDURE & VARIANTS Bone transport by illizarov is an alternative to conventional grafting
43. Fibular by pass procedure-one- or two-stage transfer (Huntington procedure and variants)
44. 7 yr/ F No involucrum one yr after onset of the disease. 2 mo post sequestrectomy/ strut graft
45. 8 mo- graft resorbed corticocancellous graft done 4 mo post grafting –fusion
46. Chronic OM with focal bone loss Small defect are managed by protection—cast or ext fixator until loss has been reconstructed In young children regeneration of entire tibial shaft has been documented Open cancellous bone graft-3- stage technique of papineau Conventional bone grafting
47. ANTIBIOTIC IMPREGNATED PMMA BEADS Delivery level of antibiotic locally in conc. that exceeds the MIC Local concentration of antibiotic are 200 times higher than systemic concentration Leaching/elution of antibiotic Heat labile/heat stable antibiotic Porous high viscosity cement surface area & elution of antibiotic Aminoglycoside /cephalosporin/ clindamycin Vancomycin- MRSA
48. Remove beads at 6 wks- Cx is foreign body formation, on which glycocalyx forming bacteria colonise & inhibit local phagocytic immune cells BIOGRADABLE ANTIBIOTIC DELIVERY SYSTEM Tobramycin-impregnated calcium sulfate pellets- only one study by Mckee VAC- aids in healing of soft tissue wounds negative pressure- wound shrinkage, resorbs fluid, granulation tissues
49. RECONSTRUCTION OF BONE DEFECT & MANAGEMENT OF DEAD SPACE Closed irrigation and suction system—ingress/ egress/ high volume irrigation/contamination risk/3-21 days Papineau tech-open cancellous bone grafting Free vascularised bone graft- fibula/ilium Well vascularised local tissue flap/free flap-used to fill dead space Bone transport or Illizarov technique
50. SOFT TISSUE COVERAGE Healing by secondary intention is to be avoided to avoid avascular scar. Types- Split thickness skin graft Local muscle flap Free vascular muscle flaps—e.g latissimus dorsi, rectus abdominus, gracilis
51. Free muscle flaps Free muscle or musculocutaneous flap-Advantages Dead space obliteration/coverage Better & easier for filling all irregular cavities Can be divided & split into exact size & form to permit transfer to bone and soft tissue defect Can be easily anchored without internal fixation FREE GRACILIS MS FLAP- harvested from opp. thigh based on its vascular pedicle- circumflex femoris medialis 60% to 100% of flap cover wounds healed compared to 40% with open cancellous bone grafting
52. Resistant chronic OM (avg. procedure per pt 2.3) Yeargan et al, J Pediatr Orthop , Volume 24, Number 1, January/February 2004
. A tibial lesion with no involucrum in a seven-year-old girl who was seen one year after onset of thedisease.Fig. 4-A: At admission, there was dislocation of the proximal tibiofibular joint, a sequestrum, bone loss of 17 per cent, and varus and flexionangulation of 10 and 25 degrees.Fig. 4-B: Two months after sequestrectomy, fibular osteotomy, and immediate grafting of the tibia with a strut graft that was obtained from the site of the ipsilateral fibular osteotomy, the graft had not been incorporated.
Eight months after the fibular cortical grafting, the graft had been resorbed and the lesion had not healed. At that time, corticocancellousiliac grafts were placed about the defect in the tibia, but the fibula was left alone.Fig. 4-D: Four months after the grafting, fusion had occurred and the position of the lateral malleolus relative to the tibia was unchanged
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