Deck 4 Flashcards
(20 cards)
Q. Describe the clinical presentation and management of suspected prosthetic infection
A. Presentation: fever, severe pain, swelling, redness
B. (History, examination, XR, FBC/ESR/CRP, microbiology culture/aspiration (prior to antibiotics)
C. Aspiration – analysis of fluid, IV antibiotics – must be done with pt off antibtiotics
D. Surgical: removal, 2 step change debridgement and retention of prosthesis, excision arthroplasty, one stage or two stage exchange arthroplasty, amputation
Q. What should Group B strep be treated with?
Amoxicillin
Q. Name two inflammatory markers
A. CRP, ESR, Alpha defensin (highly accurate in the diagnosis of prosthetic joint infection)
Q. What occurs in osteomyelitits? Who is at a higher risk?
A. Infection localised to bone
B. Increased prevalence in predisposing conditions such diabetes mellitus and peripheral vascular disease
C. Bimodal age distribution: 80% acute, haematogenous osteomyelitis occurs in children
D. Adolescent and adults get contagious osteomyelitis (associated with direct trauma)
E. Older patients: DM (diabetic), PVD, Arthroplasties
Q. Describe the clinical presentation of osteomyelitis
A. Systemic: fever, rigors, sweats, malaise
B. Local: acute (tenderness, warmth, erythema, swelling), chronic (acute signs plus draining sinus tract (formation of a passage way for pus to drain from the infected bone to the skin surface), deep/large ulcers that fail to heal despite several weeks treatment, non-healing fractures)
C. May also present as septic arthritis: when an infection breaks through cortex resulting in discharge of pus into the joint (knee, hip, shoulder) (More common in infants due to patent transphyseal blood vessels and immature growth plate)
Q. Why does osteomyelitis occur? (describe the pathogenesis)
A. Direct inoculation of infection into the bone
a. Trauma or surgery
b. Polymicrobial or monomicrobial
B. Contiguous spread of infection to bone
a. From adjacent soft tissues and joints, polymicrobial or monomicrobial,
b. Older adults: DM, chronic ulcers, vascular disease,
arthroplasties/prosthetic material
C. Haematogenous seeding,
a. Children (long bones) > adults (vertebrae)
b. Monomicrobial
D. Host factors
a. Behavioral factors: trauma risk
b. Vascular supply: arterial disease, diabetes mellitus, sickle cell disease
c. Pre-existing bone/joint problem: inflammatory arthritis, prosthetic
material
d. Immune deficiency: immunosuppressive drugs, primary
Q. What is the most common site of osteomyelitis? Why?
A. Metaphysis
B. At the metaphysis the main blood vessels penetrate the midshaft and then go to either end to form vascular loops in the metaphysis – the blood flow is slower and endothelial basement membranes are absent predisposing to transition of bacteria from the blood to this site
C. Capillaries also lack or have inactive phagocytic lining cells which allow growth of microorganisms
D. Children have a very metabolically active metaphysis (due to growing long bones) with a large flow of blood – predisposing vasculature to infection
E. Elderly: metaphysial blood flow slows with age, but the vertebrae become more vascular making bacterial seeding of vertebral endplate more likely. Also lumbar vertebral veins communicate with those of the pelvis by calce-less anastomoses.. Retrograde flow from urethral, bladder and prostatic infection may be source of bacteria to the vertebrae
Q. Which bacterium most commonly cause osteomyelitis?
A. Staph aureus, coag-negative staph (CNS), aerobic gram –ve bacilli
B. Salmonella in sickle cell, Pseudomonas aeruginosa and Serratia marcescens in
IVDU
C. Others: streptococci, enterococci, anaerobes, fungi, mycobacteria
Q. Describe two acute and two chronic changes due to osteomyelitis.
A. Acute: inflammatory cells, odema, vascular congestion, small vessel thrombosis
B. Chronic: necrotic bone ‘sequestra’, new bone formation ‘involucrum’, neutrophil exudates, lymphocytes and histiocytes
C. Inflammatory exudate in the marrow leads to increased intramedullary pressure, with extension of exudate into the bone cortex rupture through the periosteum.
Interruption of periosteal blood supply causing necrosis. Leaves pieces of separated dead bone ‘sequestra’ New bone forms here ‘involucrum’.
How should suspected OM be investigated?
D. XR, MRI, CT, ?nuclear bone scan if metalwork makes CT/MRI impossible
a. Look for cortical erosion, periosteal reaction, mixed lucency, sclerosis, sequestra, soft tissue swelling
b. MRI: marrow oedema from 3-5 days, delinates cortical, bone marrow and soft tissue inflammation
E. Diagnosis: bone biopsy, positive blood cultures
Q. What is mycobacterial osteomyelitis?
A. Extra-pulmonary TB: may have slow onset, systemic symptoms, biopsy essential
(12 month Tx)
Q. Name 2 risk factors for septic joint, How is it treated?
A. Any cause for bacteraemia, direct/penetrating trauma, local skin breaks/ulcers, damaged joints, immunosuppression, elderly, Rh arthritis, diabetes
B. Treated via repeated aspiration (rheumatology) or surgical washout (ortho)
Q. Where does sarcoma originate from, where is it found?
A. Sarcoma – mesenchymal origin (multipotent stromal cells)
B. Sarcoma is of the soft tissue (increasing incidence with age) or of the bone
(children and YP)
Q. Name two types of bone sarcoma, what age does it affect most?
A. Osteosarcoma(30%): 15-19yr olds – fast growing aggressive type – knee, thigh bone, shin bone or upper arm
B. Ewing’s sarcoma(14%): teenagers and YP, pelvis, thigh bone, shin bone – may develop into soft tissue (extraosseous sarcoma)
C. Chondrosarcoma (37%): mostly affects adults above the age of 40 – cartilage cells – upper arm, pelvis, thigh bone
D. Chordoma (^%): adults in 40s and 50s, sacrum, base of skull, spine
Q. Name two symptoms of bone sarcoma. What are the 4 key features of sarcoma presentation
A. Bone pain (nocturnal), a mass or swelling, restricted movement in a joint
B. Lump > 5cm, increasing in size, lump deep to the fascia, pain
Q. What are the main pharmacological treatments for inflammatory arthritis?
A. Analgesics and NSAIDs
B. Disease modifying drugs (DMARDS)
i. Change Progression of Disease
ii. Prevent or slow joint damage
iii. Reduce Mortality
C. Biological Agents – for severe DMARD resistant disease
Q. Name two MSK-related uses of non-steroidal anti-inflammatory drugs, name
two associated risks
A. Short term: acute gout, psuedogout
B. Long term: inflammatory arthritis, occasionally OA
C. Risks: peptic ulcers due to loss of prostaglandin protection (prescribe PPI in long-
term use), renal failure risk, may exacerbate asthma, long term use increases MI
and CVA risk
D. NSAIDS: increased BP, inhibition of prostaglandin I 2 (which inhibits platelet
aggregation)
- Q. Describe the action of corticosteroids. Name two unwanted effects.
A. Anti-inflammatory and immunosuppressive actions
B. Metabolic: DM, myopathy, osteoporosis, fat redistribution (moon face), skin
atrophy, bruising, hirsutism, acne, HTN, adrenal suppression
C. Other: infection, emotional disturbances (psychosis, depression, mania),
cataract, GI bleeding, perforation
D. Withdrawal: addisonian crisis, arthralgia/myalgia
Q. Briefly describe the mechanism of DMARDS, name two. Name two side effects
A. Distinct mechanisms for each drug, but the effect is to non specific inhibition of the inflammatory cytokine cascade – “the immune messengers”
a. Methotrexate, Sulphasalazine, Leflunomide – sometimes in combination
b. Gold injections, Azathioprine – rarely
B. DMARDS may cause the following side effects
a. Bone Marrow Suppression – low WCC, Hb, Platelets
b. Abnormal liver enzymes
c. GI effects – nausea, diarhoea
d. Oral ulceration and hair loss
e. Teratogenic to foetus (except Sulphasalazine, Azathioprine)
C. MTX: Folic acid give once weekly on different day reduces risk of side effects – due to interferences with folate metabolism
D. Leflunomide: not as well tolerated as mtx – GI side effects, very long half life, can cause HTN
E. Sulfasalazine: less effective as mtx, occasionally severe rash and neutropenia
F. Azathioprine: not usually used for RA, used mainly for SLE and vasculitis
Q. What do monoclonal antibodies target? Name two and describe two associated
side effects
A. TNF
B. Infliximab, adalimumab, rituximab
C. Side effects: increased bacterial, viral and/or fungal infections, Generation of antibodies to drugs, resulting in reduced efficacy over time
D. Drug-induced lupus-like syndromes, Emergence of lymphoma and skin cancers over long-term use
