Lecture 8 PHT2012 Osteonecrosis & Infection in ORT 20231027 .pdf

PHT2012 Orthopaedics, Traumatology & Rheumatology Lecture 9 Infection in orthopaedics. Osteonecrosis and Osteochondritis. Contents of this lecture are intended for use by BSc (Hons) students of TWC only Dr Anthony Kwok, PhD, FHKHSE, FCHSM, FAIHS, RPT Associate Professor/Deputy Programme Leader (Ph...

PHT2012 Orthopaedics, Traumatology & Rheumatology Lecture 9 Infection in orthopaedics. Osteonecrosis and Osteochondritis. Contents of this lecture are intended for use by BSc (Hons) students of TWC only Dr Anthony Kwok, PhD, FHKHSE, FCHSM, FAIHS, RPT Associate Professor/Deputy Programme Leader (Physiotherapy) School of Medical and Health Sciences 1 Read as an adjunct: Apley & Solomon’s System of Orthopeadics & Trauma: • Chapter 2 • Chapter 6 Infection in orthopaedics • A common problem associated with increased morbidity + high financial & psychosocial costs. • Incidence of infection in orthopaedic trauma patients: 5% to 10%, depending on the location and severity of the injury, and the type of #. • Recognize, prevent, diagnose & manage orthopaedics infection are utmost important, especially in the implant-related infection and the post-traumatic osteomyelitis. • Use Multilocus Polymerase Chain Reaction (MPCR) with electrospray ionization-mass spectrometry and optical imaging to diagnose the implant-related infection, and antibioticimpregnated implant coatings and cement to prevent the orthopaedics infection. • Biofilm formation on orthopaedic implants (a glycocalyx-mediated surface mode of bacterial growth) can be treated by irrigation, debridement, antibiotics or complete removal of the infected implant. • Use antibiotic-impregnated poly-methylmethacrylate (PMMA) cement beads or bio-absorbable bone substitute (BBS) delivery systems to diagnose, prevent and treat orthopaedic infection in implant-related orthopaedics infections. . Signs of wound infection 1. Fever of Over 101 F (38 C) (Marginal: 100F/37.6C) 2. Feeling of Overall Malaise/Lethargy 3. Green, Cloudy (Purulent) or Malodorous Drainage 4. Increasing or Continual Pain from Wound 5. Redness Around Wound 6. Swelling of Wounded Area 7. Hot Skin Near Wound 8. Loss of Function and Movement Recognizing Signs of Wound Infection • Highly dependent on the individual’s immune system. • Depends on whether the wound is in a high bacteria area of the body, the patient has a chronic condition (e.g. diabetes, vascular disease, poor/inconsistent wound care). • Surgical wound infection is a common hospital-acquired conditions that causes of morbidity & mortality; DIAGNOSIS OF INFECTION: No standardized protocol: • clinical evaluation, • laboratory examinations, • imaging modalities, and • intraoperative cultures. Past gold standard: • cultivation + identification of a bacterial sample from the wound. Pitfalls: • tissue-consumptive, • inaccurate in the assessment of the entire wound, • introduces the potential for specimen contamination, and • take up to 3 days before useful information becomes available. Stucken et al (2013): • retrospective reviewed f 95 nonunions in 93 patients and found that preoperative serum tests (ESR and CRP levels) were the best independent predictors of infection; • whereas nuclear imaging scans were the most expensive and least valuable tests for diagnosing infection(high specificity 92% but low sensitivity 19%). New technologies: to improve identification + localization of bacterial infections: 1. Multilocus polymerase chain reaction with electrospray ionizationmass spectrometry (PCR/ESI-MS) uses a single assay for the broad-range amplification and precise identification of many bacterial isolates, in much less time than traditional sequencing. 2. Bacterial imaging elucidates the spatial distribution of bacteria in an infection. Optical imaging of the bacteria in vivo is performed with either genetically modified bacteria encoded to emit photons, which are then quantified using a photon-counting camera or through use of a molecular probe with a fluorescent reporter group. Leevy et al (2006) introduced a near-infrared (NIR) fluorescent probe into the bloodstream of mice that had been injected with Grampositive Staphylococcus aureus, and significant accumulation at the site of the bacterial infection was noted after 18 hours. Prevention • Implant infection after Total Joint Replacement is a common mode of failure. • Incorporate antibiotics into the implant devices + antibioticimpregnated cement is commonly used to help prevent infections • Coat intramedullary (IM) rods with antibiotic polymethylmethacrylate (PMMA) cement has the added benefit of increasing stability and improve outcomes for infected nonunions of long bones, but the drug release was limited + a loss in mechanical strength for weight-bearing bone cement. • Implants with biodegradable polymer coatings can be used as controllable means to deliver antibiotics in a sustained fashion, minimizing any local or systemic toxicity associated with high fluctuating antibiotic concentrations. • Song et al (2015) used coaxial PCLCol/PVAHA nanofibers (NFs) as a nanofabricated implant coating to inhibit S. aureus infection and enhance osseointegration up to 8 weeks in a rat tibia implantation model. • They developed a calcium polyphosphate gel (CPP gel)-formulated PMMA cement, and extended the release of loaded vancomycin and tobramycin up to 25 weeks, due to the strong ionic binding of the embedded drugs with the calcium polyphosphate gel, in addition to the greater hydrophilicity and porosity of the PMMA cement, but with no significant detrimental effects on the mechanical properties of the PMMA cement. IMPLANT-RELATED INFECTION • Bacterial count for a fast flowing alpine stream at altitude is approximately 1–5 bacteria per cubic centimeter. For a square centimeter of the rock over which the stream flows, this count is 1 × 106 bacteria per cm2. • The prevalence of the glycocalyceal mode of bacterial growth causes orthopaedic implant infection and osteomyelitis. • In the glycocalyx-mediated surface mode of bacterial growth, the white cell engulfs the bacteria and the antibiotic effectiveness were compromised. The ability of Staphylococcus to reside intracellularly in an osteoblast. When the cells are killed, these cells could relinquish their Staphylococci to the surrounding tissue, making them free to grow and divide again, and causes osteomyelitic indolence. • The use of poly(lactic-co-glycolic acid) (PLGA)-based nanoparticle carrier molecules complexed to the antibiotic nafcillin was effective in allowing access to the intracellular space, whereas nafcillin alone was not. MANAGING HARDWARE-RELATED INFECTIONS 3 main factors increases the frequency and severity of hardware-related infections: 1. The presence of Methicillin-resistant S. aureus (MRSA), vancomycinresistant Enterococcus (VRE), and extended-spectrum beta-lactamase (ESBL) organisms are common. 2. The # population are older with diabetes, morbid obesity, immunosuppression, kidney disease and other chronic medical conditions. 3. A greater number of fractures are treated operatively with implants. Ways to reduce Hard-ware infection: 1. Sonication of an orthopaedic implant to remove the possible bacteria (sensitivity of cultures increased from 67% to 90%) such as MRSA or multiple organisms. 2. To improve the stability of the implanted hardware (if the implant was stable, it could be salvaged 71% of the time with irrigation, debridement, and appropriate antibiotics). Unstable or loose fixation must be removed and stability provided in another fashion (ie, external fixation). 3. The soft-tissue envelope must be evaluated as healthy coverage is a critical aspect of infection control. 4. The health of the patient should be evaluated as surgical failure rates are higher in diabetic patients with poor glycemic control, and smokers fare worse in most reviews of fracture treatment. A pre-operative smoking cessation course reduced postoperative complications from 41% to 21% (RR reduction: 49%). 5. Optimizing the patient’s health prior to intervention can improve results. 6. Application of evidence-based clinical guidelines improved the care of children with osteomyelitis through quicker diagnosis, more appropriate antibiotics, shorter admission times, and a lower readmission rate following their implementation. Osteomyelitis (OM) An infection of the bone and marrow, occurs secondary to a contiguous focus of infection; after trauma, reconstructive bone surgery, or insertion of an implant. S&S: pain in a specific bone with overlying redness, fever, and weakness. Common sites: the long bones of the arms and legs in children, and the feet, spine, and hips are common in adults. Cause: mainly bacterial infection, but occasionally fungal infection. Pathogenesis: occur by spread from the blood or from surrounding tissue. Risk factors: diabetes, intravenous drug use, prior removal of the spleen, and trauma to the area. Diagnosis: based on symptoms+ blood tests, medical imaging (Nuclear scan & MRI) or bone biopsy. Treatment: antimicrobials + surgery. In those with poor blood flow, amputation may be required. Prognosis: generally good if the condition is present a short time. Prevalence: About 2.4 per 100,000 people a year (common in the young and old). M>F. • Before the availability of antibiotics the risk of death was significant. Cause Age group Most common organisms Newborns (younger than 4 mo) S. aureus, Enterobacter species, and group A and B Streptococcus species Children (aged 4 mo to 4 y) S. aureus, group A Streptococcus species, Haemophilus influenzae, and Enterobacter species Children, adolescents (aged 4 y to adult) S. aureus (80%), group A Streptococcus species, H. influenzae, and Enterobacter species Adult S. aureus and occasionally Enterobacter or Streptococcus species Sickle cell anemia patients Salmonella species are most common in patients with sickle cell disease.[8] Classification • Based on the length of time the infection has been present + whether there is suppuration (pus formation) or sclerosis (increased density of bone) is used to arbitrarily classify OM. • Chronic OM is often defined as OM that has been present for more than one month. • A spectrum of pathologic features that reflect balance between the type and severity of the cause of the inflammation, the immune system and local and systemic predisposing factors: Suppurative osteomyelitis • Acute suppurative osteomyelitis • Chronic suppurative osteomyelitis • Primary (no preceding phase) • Secondary (follows an acute phase) Non-suppurative osteomyelitis • Diffuse sclerosing • Focal sclerosing (condensing osteitis) • Proliferative periostitis (periostitis ossificans, Garré's sclerosing osteomyelitis) • Osteoradionecrosis **OM can also be typed according to the area of the skeleton in which it is present. • Osteomyelitis of the jaws is different in several respects from osteomyelitis present in a long bone. • Vertebral osteomyelitis is another possible presentation. TREATMENT OF POST-TRAUMATIC OSTEOMYELITIS • Osteomyelitis is difficult to treat, as in its chronic form it causes devascularization of the periosteal and endosteal arterial systems, resulting in necrosis of the bone and limiting the amount of antibiotic that can be delivered systemically. • Development of a biofilm is another defining feature of chronic osteomyelitis as it increases the resistance of bacterial organisms to conventional systemic antibiotic therapy and contributes to the recurrent nature of osteomyelitis. • An integrated therapeutic treatment approach is surgical debridement of all nonviable and infected tissues followed by antimicrobial therapy (local antibiotic delivery + subsequent systemic antibiotic therapy). • Antibiotic-impregnated PMMA cement beads are used most commonly to fill the dead space resulting from debridement (disadvantages: inefficient release of antibiotic, bacterial colonization as levels of eluted antibiotic fall, and the need for a revision surgery to remove the PMMA beads) • Incorporated xylitol into daptomycin-impregnated PMMA to increase the porosity of PMMA and enhance its elution profile. Incorporation of xylitol is able to prolong the release of antibiotic. • a bioabsorbable bone substitute (BBS) delivery vehicle that included tobramycin-impregnated medical-grade alpha-hemihydrate calcium sulfate resulted in the eradication of infection in 86% of patients (with new bone growth and decreased rate of secondary surgical procedures + associated complications). Osteonecrosis (ON)/Avascular Necrosis (AVN)/ Aseptic Necrosis(AN) • Osteonecrosis is the death of bone cells due to decreased blood flow, leading to pain and collapse of areas of bone, eventually lead to degenerative arthritis(OA) of nearby joints. • Osteonecrosis can lead to pain, arthritis and limited use of affected joints. Some people may even need joint replacement surgery. • Early diagnosis and early treatment may improve the outcome. Steinberg staging of avascular necrosis of hip (similar to the Ficat & Arlet staging). • Based on the radiographic appearance and location of lesion (differs from the other systems by quantifying the involvement of femoral head) • Following staging, extent of involvement of femoral head is recorded as mild, moderate or severe. Classification stage 0: normal or non-diagnostic radiographs, MRI and bone scan of at risk hip (often contralateral hip involved, or patient has risk factors and hip pain) stage I: normal radiograph, abnormal bone scan and/or MRI stage II: cystic and sclerotic radiographic changes stage III: subchondral lucency or crescent sign stage IV: flattening of femoral head, with depression graded into • mild: <2 mm, moderate: 2-4 mm, severe: >4 mm stage V: joint space narrowing with or without acetabular involvement stage VI: advanced degenerative changes Quantification of extent of involvement is necessary for stages I to V: stage I and II • A, mild: <15% head involvement as seen on radiograph or MRI • B, moderate: 15% to 30% • C, severe: >30% stage III • A, mild: subchondral collapse (crescent) beneath <15% of articular surface • B, moderate: crescent beneath 15% to 30% • C, severe: crescent beneath >30% stage IV • A, mild: <15% of surface has collapsed and depression is <2 mm • B, moderate: 15% to 30% collapsed or 2-4 mm depression • C, severe: >30% collapsed or >4 mm depression stage V • A, B or C: average of femoral head involvement, as determined in stage IV, and estimated acetabular involvement The Ficat and Arlet classification (uses a combination of plain radiographs, MRI, and clinical features to stage avascular necrosis of the femoral head). Stage 0: plain radiograph: normal, MRI: normal, clinical symptoms: nil stage I: plain radiograph: normal or minor osteopenia, MRI: edema, bone scan: increased uptake • clinical symptoms: pain typically in the groin stage II: plain radiograph: mixed osteopenia and/or sclerosis and/or subchondral cysts, without any subchondral lucency (crescent sign: see below) • MRI: geographic defect, Bone Scan: increased uptake • clinical symptoms: pain and stiffness stage III: plain radiograph: crescent sign and eventual cortical collapse • MRI: same as plain radiograph • clinical symptoms: pain and stiffness +/- radiation to knee and limp stage IV: plain radiograph: end-stage with evidence of secondary degenerative change, • MRI: same as plain radiograph • clinical symptoms: pain and limp • Most often in hips, knees (weight bearing); less often in the shoulders, hands and feet (non-weight bearing); and rarely in the jaw (osteonecrosis of Jaw, ONJ, can be resulted from ulcers (sores) of gum tissue (exposed jaw bone and pain) with the prolonged taking of Bisphosphonates (osteoporosis anti-resorptive drugs, such as Fosamax, Actonel or Bonviva). • Osteonecrosis may result from use of glucocorticoid (corticosteroid) medicine (such as the SARS survivors in 2003, or RA/SLE patients ) or from drinking too much alcohol. Common causes of osteonecrosis: • Serious trauma/injury that interrupts a bone’s blood supply • Corticosteroid medications (e.g. prednisone, cortisone or methylprednisolone), mainly when a high dose is used for a prolonged period of time • Excess alcohol consumption • Systemic lupus erythematosus (SLE) Other risk factors: • pression disease (also called the “Bends” in the scuba diving) • Blood disorders such as sickle cell anemia, antiphospholipid antibody syndrome (APS) and lupus anticoagulant • HIV infection (AIDS) • Radiation therapy • Bisphosphonates, which may be linked to osteonecrosis of the jaw • Organ transplants Around 10,000 to 20,000 Americans, between the ages of 20 and 50, develop osteonecrosis each year. Most often have a history of serious trauma, corticosteroid use, excess alcohol intake or other risk factors. • Doctors suspect osteonecrosis when a person with risk factors for it feels bone pain that is “localized” (limited to a small area). • Patients with hip pain due to osteonecrosis often feel pain in the groin, and is most often worse with weight-bearing/walking. Diagnosis: X-ray of the painful area (may look normal in the early stages of disease), bone scans or MRI (excellent in detecting early osteonecrosis). Osteonecrosis of the jaw (may be due to taking of bisulphonates in poor oral hygiene patients) Management: • No clear proof of the best management. • Early treatment (before bone collapse) is best. Early treatment: pain medications + limiting weight-bearing/walking (NWB/PWB) on affected areas: • work well for patients with early osteonecrosis in small areas of bone. • For hip or knee osteonecrosis patients with worsening disease and bone collapse, they may need surgical procedures to relieve pain and to prevent bone collapse. Surgery: i) core decompression (removes a piece/core of bone from the affected area to improve blood flow). ii) More advanced cases: osteotomy (remove dead bone and re-position the remaining bone so that healthy bone supports the weight-bearing joint surface). iii) If bone collapse at the joint has occurred, total joint replacement (arthroplasty) of the hip or knee (improve pain and function). iv) Another surgery option for advanced cases: bone grafting (take a small piece of a person’s own healthy leg bone and graft (transplanting) it to the area of dead bone to improve blood flow and support of the surrounding bone. Medicine: no proven medical therapy for ON/AVN. Some studies suggest that short-term bisphosphonate treatment may slow/improve/prevent bone collapse in the hip and knee. Prevention: i). To avoid too much alcohol intake and avoid tobacco use ( smoking raises the risk of osteonecrosis). ii). If you have to take corticosteroids, such as prednisone, work with your doctor to take the smallest dose for the shortest time possible that will control your symptoms. Living with osteonecrosis: Some people will develop OA. PT for treating the pain + joint stiffness + ambulation. Partial weight exercises like the hydrotherapy/cycling is good for the AVN patients. Osteochonditis/osteochondritis dissecans (OCD) 1. Osteochonditis: a painful type of osteochondrosis (the cartilage/bone in a joint is inflamed). 2. Osteochondritis dissecans (OCD): i) dissecans means the "creation of a flap of cartilage that further dissects away from its underlying subchondral attachments". ii) osteochondritis are osteochondritis deformans juvenilis (e.g. osteochondritis of the capitular head of the epiphysis of the femur) and osteochondritis deformans juvenilis dorsi (e.g. osteochondrosis of the spinal vertebrae/ Scheuermann's disease). Osteochondritis dissecans (OCD): • A joint condition: bone underneath the cartilage of a joint dies due to lack of blood flow → this bone and cartilage can then break loose, causing pain and possibly hindering joint motion. • Occurs often in children and adolescents. • Commonly in the knee, elbows, ankles and other joints. S&S: According to the size of the injury + whether the fragment is partially or completely detached + whether the fragment stays in place. 1. If the loosened piece of cartilage and bone stays in place: few or no symptoms. 2. For young children whose bones are still developing, the injury might heal by itself. 3. Symptoms either after an injury to a joint or after several months of activity (as in high-impact activity: jumping and running that affects the joint). 4. Depending on the joint affected): • Pain on weight bearing/physical activity (e.g. walking up stairs, climbing a hill or playing sports). • Swelling + tenderness in the skin around the affected joints. • Joint effusion + unstable: popping/locking, "giving way“/ weakening. • Decreased ROM: unable to straighten the affected limb completely. • Common in knee, elbow, ankles and the other joints that move often. Causes: unknown. • i). Probably due to the reduced blood flow to the end of the affected bone might result from repetitive trauma (small, multiple episodes of minor, unrecognized injury that damage the bone). • ii) genetic component: some people more prone to develop the disorder. Risk factors: in children and adolescents between the ages of 10 and 20 who are highly active in sports. Complications: can increase the risk of developing OA in that joint. Surgery is necessary if the fragment comes loose and gets caught between the moving parts of your joint or on persistent pain. Prevention (Adolescents participating in organized sports): i). educate on the risks to their joints associated with overuse. ii). Learn the proper mechanics and techniques of their sport iii). Use the proper protective gear iv). Participate in strength training + stability training exercises to reduce the chance of injury. Septic arthritis/joint infection/infectious arthritis The invasion of a joint by an infectious agent resulting in joint inflammation. Symptoms: redness, heat and pain in a single joint associated with a decreased ability to move the joint + onset rapid. Fever, weakness and headache. Occasionally, > 1 joint may be involved. Causes: bacteria, viruses, fungi and parasites. Risk factors: an artificial joint, prior arthritis, diabetes and poor immune function. Occurrence: joints become infected via the blood, via trauma or via an infection around the joint. Dx: joint aspiration + culture (joint fluid): +ve if WBC > 50,000 mm3, lactate > 10 mmol/l in the jt. Initial treatment: antibiotics such as vancomycin, ceftriaxone or ceftazidime. Surgery: to clean out the joint. Without early treatment, long-term joint problems may occur. Septic arthritis occurs in about 5 people per 100,000 each year (common in older people). With treatment: 15% of people die Without treatment: 66% die. Signs and symptoms • Pain + swelling + warmth at the affected joint. • Refuse to use the joint/joint rigidly + Fever (less likely in older adults). • P/E to rule out of intra-articular or periarticular cause. Intra-articular arthritis usually results in severe limitation of the ROM of the joint with the joint held in extended position; the joint space will be maximal in this position. In peri-articular arthritis, pain only occurs when the joint is moved, and the lesion usually lies in one specific area around the joint. • Knee is more affected. Hip, shoulder, wrist and elbow joints are less common. • Spine, Sternoclavicular Joint and SIJ can also be involved (due to IV drug use). • Usually, only 1 joint is affected. • > 1 joint are spread through the bloodstream. Prosthetic joint Infections 0.86 - 1.1% in a Knee joint, 0.3 - 1.7% of in a hip joint. 3 phases of artificial joint infection: 1. Early: occurs < 3/12 after the surgery. S&S: fever, joint pain, redness + warmth over the joint operation site. Usual bacteria: Staphylococcus aureus and gram negative bacilli. 2. Delayed: occurs between 3 – 24/12. S&S: persistent joint pain, due to loosening of the implant. Common bacteria: coagulase-negative Staphylococcus and Cutibacterium acnes. 3. Late: > 2 years. S&S: sudden onset of joint pain + fever. The mode of infection is through the bloodstream. The bacteria involved are the same as those in septic arthritis of a normal joint. Cause: by a bacterial infection. Bacteria can enter the joint by: • The bloodstream from an infection elsewhere (most common) • Direct penetration into the joint (arthrocentesis, arthroscopy, trauma) • A surrounding infection in the bone or tissue (from osteomyelitis, septic bursitis, abscess). • Microorganisms in the blood may come from infections elsewhere in the body such as wound infections, urinary tract infections, meningitis or endocarditis. Infection also comes from an unknown location. Risk factors: • Age over 80 years • Diabetes mellitus • OA • RA (increases with anti-tumor necrosis factor alpha treatment). • Immunosuppressive medication • Intravenous drug abuse • Recent joint surgery • Hip or knee prosthesis and skin infection • HIV infection • Other causes of sepsis HIV (Human Immunodeficiency Virus) Surveillance at a glance in HK (2016) 692 HIV reports and 111 AIDS (Acquired Immune Deficiency Synfrome) reports Gender: 86.1% male, Ethnicity: 73.0% Chinese, Age: Median 35 Risks: • 63.7% Homosexual/bisexual contact • 21.1% Heterosexual contact • 0.9% Injecting drug use • 14.3% Undetermined CD4 at reporting: Median 284/ul HIV-1 subtypes: commonest are CRF01_AE and B • Commonest primary AIDS defining illness: PCP (Angel Dust) and TB HIV prevalence • Blood donors: <0.01%, Antenatal women: 0.02%, STI clinic attendees: 0.48%, Methadone clinic attendees: 1.13% Causative Organisms: 1. Most involve only 1 organism 2. Polymicrobial infections in a large open injuries to the joint 1. Mainly caused by bacteria, 2. But may be caused by viral, mycobacterial, and fungal pathogens. Classification: 3 main groups 1. Non-gonoccocal arthritis: over 80% are staphyloccoci or streptococci (from drug abuse, cellulitis, abscesses, endocarditis, and chronic osteomyelitis. Methicillin-resistant Staphylococcus aureus (MRSA) may affect 5 to 25% of the cases while gram negative bacilli affects 14 to 19% of the septic arthritis cases. Gram negative infections are usually acquired through urinary tract infections, drug abuse, and skin infections. Old people who are immunocompromised are also prone to get gram negative infections. Common gram negative organisms are: Pseudomonas aeruginosa and Escherichia coli. Both gram positive and gram negative infections are commonly spread through the blood from an infective source; but can be introduced directly into the joint or from surrounding tissue. 2. Gonococcal arthritis : Neisseria gonorrhoeae is a common cause of septic arthritis in people who are sexually active and under 40 years old. The bacteria is spread through the blood to the joint following sexual transmission. 3. Others : Fungal and mycobacterial infections are rare with a slow onset of joint symptoms. Viruses such as rubella, parvovirus B19, chikungunya, and HIV infection can also cause septic arthritis. Prosthetic joint infection: 1. Staphylococci, 2. Staphylococcus aureus, 3. gram negative bacilli. The risk factors: Previous fracture, Seropositive rheumatoid arthritis, Obesity, Revision arthroplasty, and Surgical site infections. List of organisms (1) • Staphyloccoci (40%) • Staphylococcus aureus – the most common cause (in skin infection, previously damaged jt, prosthetic jt or IV drug use). • coagulase-negative staphylococci – usually due to prosthetic joint • Streptococci – the second-most common cause (28%) • Streptococcus pyogenes – a common cause in children under 5 • Streptococcus pneumoniae • Group B streptococci – a common cause in infants • Haemophilus influenzae List of organisms (2) • Neisseria gonorrhoeae –in young, sexually active adults (Multiple macules or vesicles seen over the trunk are a pathognomonic feature). • Neisseria meningitidis • Escherichia coli – in the elderly, IV drug users and the seriously ill • Pseudomonas aeruginosa – IV drug users or penetrating trauma through the shoe • M. tuberculosis, Salmonella spp. and Brucella spp. – cause septic spinal arthritis • Eikenella corrodens – human bites • Pasteurella multocida, bartonella henselae – animal bites or scratches • Fungal species – immunocompromised state • Borrelia burgdorferi – ticks, causes lyme disease Diagnosis • Considered whenever a person has rapid onset pain + swollen joint, regardless of fever (one or multiple joints can be affected at the same time). • P/E + arthrocentesis: joint fluid culture + blood cultures • WBC count, ESR, CRP, VDRL • In children: Kocher criteria is used for diagnosis of septic arthritis • Gram stain: Synovial fluid cultures are +ve in over 90% of nongonoccocal arthritis (may be -ve if the person received antibiotics prior to the joint aspiration, or in gonoccocal arthritis, or if fastidious organisms are involved). • Positive crystal studies do not rule out septic arthritis, as gout can occur at the same time as septic arthritis. • A lactate level in the synovial fluid of greater than 10 mmol/l makes the diagnosis very likely. • Blood tests: WBC count, ESR and CRP elevated in septic arthritis. • Blood cultures can be +ve in up to 50% septic arthritis cases. • Imaging: x-ray, CT, MRI or US are nonspecific (good in determining the areas of inflammation but cannot confirm septic arthritis). • US is effective at detecting joint effusions and are helpful in guiding arthrocentesis of the joints. Differential diagnosis • Crystal induced arthritis such as gout or pseudo-gout • Inflammatory arthritis • Rheumatoid arthritis • Seronegative spondylo-arthropathy such as ankylosing spondylitis or reactive arthritis • Traumatic arthritis due to hemarthrosis, fracture or foreign body • Osteoarthritis Treatment • Intravenous antibiotics, analgesia and washout +/- aspiration of the joint. • Draining the pus from the jt. by needle (arthrocentesis)/opening the joint surgically (arthrotomy). Empiric antibiotics for suspected bacteria as follows: • Gram positive cocci – vancomycin; Gram negative cocci – Ceftriaxone • Gram negative bacilli – Ceftriaxone, cefotaxime, or ceftazidime • Gram stain negative and immunocompetent – vancomycin • Gram stain negative and immunocompromised – vancomycin + third generation cephalosphorin • IV drug use (possible pseudomonas aeruginosa) – ceftazidime +/- an aminoglycoside • Once cultures are available, antibiotics can be changed to target the specific organism. After a good response to IV antibiotics → switch to oral antibiotics (1–4 weeks depending on the offending organism). • Daily joint aspiration + aspirate sent for culture, gram stain, white cell count to monitor the progress. • Open surgery/Arthroscopy (including lysis of the adhesions, drainage of pus, and debridement of the necrtoic tissues). • Close follow up to make sure the patient is no longer feverish, pain has resolved, improved ROM, and lab values are normalized. • In infection of a prosthetic joint, a biofilm is often created on the surface of the prosthesis which is resistant to antibiotics. Surgical debridement is indicated. • A replacement prosthesis is not inserted at the time of removal to allow antibiotics to clear infection of the region. • Low-quality evidence suggests that the use of corticosteroids may reduce pain and the number of days of antibiotic treatment in children. Osteochondritis or Osteochondritis Dissecans, OCD. • A painful type of osteochondrosis where the cartilage or bone in a joint is inflamed. • Osteochondritis Dissecans: Dissecans means the "creation of a flap of cartilage that further dissects away from its underlying subchondral attachments (dissecans). Other types: • osteochondritis deformans juvenilis (osteochondritis of the capitular head of the epiphysis of the femur) and • osteochondritis deformans juvenilis dorsi (osteochondrosis of the spinal vertebrae, or Scheuermann's disease). Osteochondritis deformans juvenilis A temporary condition in children in which the femoral head loses its blood supply: the femoral head collapses. • Follow on: the body will absorb the dead bone cells and replace them with new bone cells. The new bone cells will eventually reshape the femoral head. S&S: causes the hip joint painful and stiff for a period of time. The majority of cases affect 1 hip; 10-12 % of cases affect both hips. Risk factors: more common in boys (5:1 male-female ratio). • Association of osteochondritis deformans juvenilis with ADHD (attention deficit hyperactivity disorder) and in children who are more active than average (running, jumping, sports, etc). • An increased incidence in children who are small for their age (delayed bone age). • Recent studies that connect osteochondritis deformans juvenilis to prolonged exposure to second hand smoke: prolonged inhalation of cigarette smoke increases the risk of ischemia leading to the osteochondritis deformans juvenilis. Common in the Asian, Eskimo, and Caucasian population. Treatment: supportive therapy and ensure your child's hip retains its normal shape and ROM. Scheuermann's disease • A self-limiting skeletal disorder of childhood. • A condition where the vertebrae grow unevenly with respect to the sagittal plane; that is, the posterior angle is often greater than the anterior. • This uneven growth results in the signature "wedging" shape of the vertebrae, causing kyphosis. S&S: • A form of juvenile osteochondrosis of the spine in teenagers and presents a significantly worse deformity than postural kyphosis. • Scheuermann’s kyphosis: the apex of their curve, located in the thoracic vertebrae, is quite rigid. • Pain in the lower & mid-level back and neck : severe and disabling, aggravated by physical activity and by periods of standing or sitting. • May cause detrimental effect and disability. • Loss of vertebral height, and 'hunchback'/'roundback'. • The 7th and 10th thoracic vertebrae are commonly affected. • In very serious cases: may cause internal organ problems and spinal cord damage, but extremely rare. Management: Physiotherapy for mild case and surgery for sever cases. Chondromalacia • A condition where the cartilage on the undersurface deteriorates and softens • Often seen as an overuse injury in sports • Sometimes taking a few days off from training can produce good results. • Improper knee alignment is the cause and if resting doesn’t provide relief. • The symptoms of runner’s knee are knee pain and grinding sensations • Many people may have it without seeking medical treatment. Chondromalacia patellae (CMP) • A condition where the cartilage on the undersurface of the patella deteriorates and softens. • Also known as Runner Knee. S&S: Pain and discomfort in the patellofemoral joint. The patella may be laterally rotated or tilted. Tight musculatures around the Knee region. Staitrs walking: Pain in downstairs > upstairs). Patellar Friction Test: +ve Prevalence: commonly in young females, young athletic, or in older adults with arthritis of the knee. Dx: Knee Physical examination + XR: Skyline Laurin view in NWB position. Skyline Laurin view Understanding the different locations of Knee Pain Causes: 1. When the knee bends, the retro-patellar surface glides over the cartilage of the femur at the knee in a normal “tracking format”. 2. When the ITB, Hamstrings, Quadriceps, calf tendons and the ligaments around the Knee are tight 3. When any of these components fails to move properly, it can cause the patella to rub up against the femur. 4. The abnormal rubbing can lead to deterioration in the patella, resulting in chondromalacia patellae, or runner’s knee. Improper Patella tracking movement may be resulted from: • poor alignment due to a congenital condition • weak hamstrings and quadriceps • Muscle imbalance between the adductors and abductors (e.g. ITB and Adductor Magnus) • Repeated stress to the knee joint such as from running, skiing, or jumping • A direct blow or trauma to the patella Risk for developing chondromalacia patellae (CMP) 1. Age: Adolescents and young adults at high risk - during growth spurts, the muscles and bones develop rapidly, which may contribute to short-term muscle imbalances. 2. Gender: Females >> males to develop runner’s knee. Less muscle mass in females may cause abnormal knee positioning and more lateral (side) pressure on the patella. 3. Flat feet: place more stress on the knee joints than having higher arches would. 4. Previous injury: prior injury to the patella, e.g. dislocation, may increase the risk of developing runner’s knee. 5. High activity level: place extra pressure on the knee joints, and increase the risk for knee problems. 6. Arthritis Runner’s knee can also be a symptom of arthritis. Inflammation can prevent the kneecap from functioning properly. CMP Management • NSAID • Analgesic Physiotherapy: Stretches to Hamstrings, Quadriceps, ITB, Hip adductors, calves. • Treat the flat foot • Strengthening exercises: Quadriceps and Hamstring • Stretches to tight musculatures around the Knee region • Jenny McConnell Exercises to PFJP • Patellar taping • Home programme and advice References 1. Blom, A., Warwick, DJ, & Whitehouse, M.. (2018). Apley & Solomon’s System Of Orthopaedics And Trauma. (10th ed.). Florida, CRC Press. 2. Cook, G.; Markel, D.; Ren, W.; Lawrence M.; Schemitsch, E. (2015), “Infection in orthopaedics”, Journal of Orthopaedic Trauma: Dec 2015, Vol 29, Issue p S19–S23. 3. Frontera, W. R., Silver, J. K., & Rizzo, T. D. (2018). Essentials of Physical Medicine and Rehabilitation: Musculoskeletal Disorders, Pain and Rehabilitation. (4th ed.). Philadelphia: W.B. Saaunders Company. 4. Goodman, C & Fuller, K (2015). Pathology: implications for the physical therapist. St. Louis, MO: Elsevier Saunders. 5. Leevy WM, Gammon ST, Jiang H, et al.. Optical imaging of bacterial infection in living mice using a fluorescent nearinfrared molecular probe. J Am Chem Soc. 2006;128:16476–16477. 6. Porter, S. (2013), Tidy's Physiotherapy, 15e (Physiotherapy Essentials). 7. Porter, R. (2018), The Merck Manual of Diagnosis & Therapy (20th edition), Weiley 8. Photos from Google web pages. 9. Song W, Seta J, Kast RE, et al.. Influence of particle size and soaking conditions on rheology and microstructure of amorphous calcium polyphosphate hydrogel. J Am Ceram Soc. 2015. 10. Stucken C, Olszewski DC, Creevy WR, et al.. Preoperative diagnosis of infection in patients with nonunions. 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