BONE AND JOINT INFECTION. Dr.Jónás Zoltán Dept.of Orthopaedics
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1 BONE AND JOINT INFECTION Dr.Jónás Zoltán Dept.of Orthopaedics
2 Order of verbal exams: The students are able to register for the exam on the Neptun system. The students pick two titles, from the title list available at the beginning of the Semester. This list can be also found on the web site of the Orthopaedic Department. Those students who attended at least 70 % of the lectures will pick two titles, but will only be examined on the one of their choice. In case of a B or C exam the student is not entitled to the above advantage.
3 TERMINOLOGY INFECTION OF THE BONE: OSTEOMYELITIS INFECTION OF THE JOINT: SEPTIC ARTHRITIS
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5 Outcome of bone infection 1.Virulence of bacteria depends on two factors: 2.Resistance (defensive ability) of the host If virulence is high or resistance is low-acute. If virulence is low or resistance is high-chronic.
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8 ACUTE HAEMATOGENOUS OSTEOMYELITIS Most important form.(model for other forms of bone infections). Bacteria reach the bones from a distant infected site of the body via the blood stream. Mainly children are affected. If adults - their resistance are lowered (diabetes,immunosuppression,organ transplantation,systemic steroid medication,aids,etc.)
9 ACUTE HAEMATOGENOUS OSTEOMYELITIS ETIOLOGY Most frequent causative organisms: (staphylococci, (mainly S.aureus), streptococci (young children), pneumococci, H.influenzae. FOCI ( distant infected site): Otitis, infected umbilical cord, tonsillitis, urinary tract, pyoderma
10 S.aureus
11 S.aureus
12 STEPS OF BONE INFECTION I.Blood stream infection and bacterial settlement in the bone II. -inflammation (colonization) -local infective thrombosis, toxins,intraosseal pressure raises rapidly./1-2 day/ -suppuration (pus formation) -subperiosteal abscess formation /3-4 day/ -necrosis (bone death)-sequester formation /by 1 week/ -new bone formation (involucrum) - periosteal strippingcambium layer /by 2 week/ -resolution (remodelling).
13 STEPS OF BONE INFECTION I.Blood stream infection and bacterial settlement in the bone II. -inflammation (colonization) -local infective thrombosis, toxins,intraosseal pressure raises rapidly./1-2 day/ -suppuration (pus formation) -subperiosteal abscess formation /3-4 day/ -necrosis(bone death)-sequester formation /by 1 week/ -new bone formation (involucrum) - periosteal strippingcambium layer /by 2 week/ -resolution (remodelling).
14 inflammation(colonization)
15 STEPS OF BONE INFECTION I.Blood stream infection and bacterial settlement in the bone II. -inflammation (colonization) -local infective thrombosis, toxins, intraosseal pressure raises rapidly./1-2 day/ -suppuration (pus formation) -subperiosteal abscess formation /3-4 day/ -necrosis(bone death)-sequester formation /by 1 week/ -new bone formation (involucrum) - periosteal strippingcambium layer /by 2 week/ -resolution (remodelling).
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17 STEPS OF BONE INFECTION I.Blood stream infection and bacterial settlement in the bone II. -inflammation (colonization) -local infective thrombosis, intraosseal pressure raises rapidly./1-2 day/ -suppuration (pus formation) -subperiosteal abscess formation /3-4 day/ -necrosis(bone death)-sequester formation /by 1 week/ -new bone formation (involucrum) - periosteal strippingcambium layer /by 2 week/ -resolution (remodelling).
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20 Orthopaedic infections in children ACUTE HAEMATOGENOUS OSTEOMYELITIS Pathology 1. Inflammation (colonization)-bacterial embolization and infected thrombosis Acute inflammatory reaction with vascular congestion Rise in intra-osseous pressure causing intense pain 2. Suppuration At 3-4 days pus forms within the bone and forces its way down the haversian canals to the surface where it forms a sub-periosteal abscess The pus can spread from here back into the bone, into an adjacent joint or into the soft tissues (Where there is an intra-articular metaphysis - prox.femur, prox.humerus,prox.radius- joint involvment!!!) Vertebral infection can spread through the end plate, disc and into the next vertebral body 3. Necrosis At 7 days, rising pressure, vascular stasis, infective thrombosis and periosteal stripping and toxins compromise the blood supply to the bone resulting in bone death which results in a sequestrum. 4. New bone formation At days this forms from the deep surface of the stripped periosteum forming the involucrum 5. Resolution With release of the pressure and appropriate antibiotics healing can occur There may be permanent deformity Unpublished work (quoted in Dee) shows that experimentally bacteria injected intravenously will settle in the metaphyses of bone preferentially NB - in 10% of cases there is more than one site of infection. Clinical Features Children (invariably) Pain, malaise, fever Limp or not weight bearing Infants Failure to thrive, drowsiness, irritable Adults The commonest site is the thoracolumbar spine (Batson's venous complex from the pelvis) Other bones involved especially in DM, IVDA, immunosuppressed Examination Local erythema, swelling and tenderness indicates that the pus has broken through the periosteum
21 ACUTE HAEMATOGENOUS OSTEOMYELITIS- PATHOGENESIS Localisation: metaphysis Special vascular pattern (non-anastomosing terminal branches), slow blood flow, growing cells are vulnerable for infection
22 ACUTE HAEMATOGENOUS OSTEOMYELITIS- CLINICAL FEATURES Rapid onset Generally bad condition Fever GENERAL SIGNS OF INFECTION: Pain (dolor) Redness (rubor) Swelling (tumor) Warmth (calor) Restricted movements (functio laesa)
23 BONE and JOINT INFECTIONS- laboratory investigations ESR- (100 mm/h) CRP- elevated Blood culture Aspiration (gram stain,culture, antibiogram)
24 ACUTE HAEMATOGENOUS OSTEOMYELITIS- IMAGING PLAIN X-RAY Periosteal new bone (10-14 days postinfection, too late) RADIOISOTOPE UPTAKE Very sensitive but not specific MRI ULTRASOUND
25 ACUTE HAEMATOGENOUS OSTEOMYELITIS- IMAGING PLAIN X-RAY Periosteal new bone (10-14 days postinfection, too late) RADIOISOTOPE UPTAKE Very sensitive but not specific MRI ULTRASOUND
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28 sequester
29 ACUTE HAEMATOGENOUS OSTEOMYELITIS- IMAGING PLAIN X-RAY Periosteal new bone (10-14 days postinfection, too late) RADIOISOTOPE UPTAKE Very sensitive but not specific MRI ULTRASOUND
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31 ACUTE HAEMATOGENOUS OSTEOMYELITIS- IMAGING PLAIN X-RAY Periosteal new bone (10-14 days postinfection, too late) RADIOISOTOPE UPTAKE Very sensitive but not specific MRI ULTRASOUND
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33 STEPS OF BONE INFECTION- TREATMENT I.Blood stream infection (bacteriaemia) and bacterial settlement in the bone ANTIBIOTICS II. inflammation (colonization) -local infective thrombosis,intraosseal pressure raises rapidly /1-2 day/ DRILLING suppuration (pus formation) -subperiosteal abscess formation /3-4 day/ EVACUATION and DRILLING necrosis (bone death) -sequester formation /by 1 week/ CURETTAGE and SEQUESTRECTOMY new bone formation (involucrum)-periosteal stripping -cambium layer /by 2 week/ CURETTAGE and SEQUESTRECTOMY resolution (remodelling)
34 ACUTE HAEMATOGENOUS OSTEOMYELITIS- COMPLICATIONS METASTATIC INFECTION SUPPURATIVE ARTHRITIS GROWTH DISTURBANCIES ( altered length, axial deformities) CHRONIC OSTEOMYELITIS LETHAL OUTCOME
35 SUBACUTE FORMS Virulence of bacteria is not high. Defensive ability of host is good. X-ray: well-defined laesion surrounded by sclerotic rim. Means differential diagnostic problems. Needs no surgery (if dg.is sure), antibiotic treatment alone is sufficient.
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37 BRODIE ABSCESS
38 CHRONIC FORMS
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40 Outcome of bone infection 1.Virulence of bacteria depends on two factors: 2.Resistance (defensive ability) of the host If virulence is high or resistance is low-acute. If virulence is low or resistance is high-chronic.
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43 Treatment of chronic osteomyelitis Almost exclusively surgical : radical debridement (mechanical removal of infected tissues)
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47 Antibiotic-loaded spacer
48 Modellált, ragasztott gyári spacer
49 SEPTIC ARTHRITIS Route of spread Haematogenous (infected umbilical cord,otitis,tonsillitis,etc.). Spread from metaphyseal osteomyelitis where the metaphysis is intra-articular (prox.femur,prox.humerus,prox.radius). Spread from contiguous soft tissue infection. Direct inoculation. Spread through the growth plate(infants!)
50 SEPTIC ARTHRITIS ETIOLOGY Most frequent causative organisms: (staphylococci, streptococci (young children), pneumococci, E.coli Bacteria settle down in the synovial membrane. Cartilage and bone also can be affected.
51 Rapid onset Fever SEPTIC ARTHRITIS- CLINICAL FEATURES GENERAL SIGNS OF INFECTION: Pain (dolor) Redness (rubor) Swelling, fluctuation (tumor) Warmth (calor) Restricted movements (functio laesa)
52 ESR- (100 mm/h) CRP- elevated Blood culture SEPTIC ARTHRITIS- LABORATORY FEATURES Aspiration (gram stain,culture, antibiogram)
53 SEPTIC ARTHRITIS- TREATMENT ANTIBIOTICS, ANALGESICS, SPLINTAGE ASPIRATION (repeated) DRAINAGE CONTINUOUS SUCTION-IRRIGATION SYNOVECTOMY CORRECTIVE OSTEOTOMY ARTHRODESIS
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