Soft tissue, bone and joint infections Flashcards
What is the aim of the skin and what are its 3 main layers?
physical barrier against microorganisms
3 layers:
1) epidermis: outer layer and waterproof
2) dermis: tough connective tissue, hair follicles and sweat glands
3) subcutaneous layer: fat and connective tissue
What are the non-specific defences of skin?
exfoliation: sloughing of the stratum corneum dislodges many adherent bacteria
dryness: bacterial counts much higher in moist areas
acidic: pH 5.5
low temperature
sweat glands: saltiness - inhibits bacteria
normal bacterial flora - complete for colonisation sites, compete for nutrients
What is the normal flora of the skin?
microorganisms are always present on the skin
- s epidermidis
- s aureus
- micrococci
- diphtheroids
some microorganisms are transient flora and are prevented from colonising due to:
- mechanical barrier
- sebum
- cleaning and washing
What type of organism is staphylococcus aureus?
gram +ve cocci and coagulase positive golden colonies - yellowy/cream colour 30-40% of population are colonised acquired resistance to beta-lactam antibiotics - methicillin causes haemolysis of red cells
What type of organism is streptococcus pyogenes?
group A streptococci
gram +ve cocci
beta haemolytic - get partial haemolysis of alpha chains
colonises the pharynx
What syndromes do you get within the epidermidis and dermis?
impetigo folliculitis furunculosis carbunculosis erysipelas \+ cellulitis
What syndromes do you get within the superficial fascia, subcutaneous fat, nerves, arteries, veins and deep fascia ?
necrotising fascitis
What syndrome do you get in the muscle?
myonecrosis
What conditions predispose to skin invasion?
excessive moisture - induces breakdown of the stratum corneum - occlusive dressings, obesity (infections seen in intertriginous folds)
minor abrasions
surgery
crush injuries - RTAs
burns - infections primary cause of death in burns patients
percutaneous e.g. intravenous catheters
bed sores- cutaneous lesions due to pressure lead to skin necrosis and secondary infections
conditions that compromise the blood supply- diabetes
What is impetigo?
superficial skin infection friable golden crusts over erythematous skin more common in children very contagious usually due to strep A
What is folliculitis?
infection of the hair follicles
common sites are groin and scalp
causative organism= s aureus
tx= flucloxacillin
What are some pyogenic skin infections?
furunculosis = deep inflammatory lesion progressing from a folliculitis
carbuncle = multiple fistulas = extend into the subcutaneous layer, multiple abscesses develop, separated by connective tissue
acute paronchia = skin infection arising from nail - remove nail and pus pores out
tx= oral flucloxacillin
What is cellulitis?
acute, spreading inflammation of the lower dermis and associated with subcutaneous layer of skin
diffuse inflammation without necrosis or localisation of pus
often seen as red halo around wound
skin is hot, red and painful
What is the causative agent of cellulitis commonly ?
s. aureus
less common- s pyogenes, c perfringens
How is cellulitis diagnosed?
most commonly affects lower extremities
acute, tender, erythematous and swollen area of skin - could be a DVT
fever and malaise
WCC and CRP usually raised
blood cultures only useful if pt is septic
What is the treatment for cellulitis?
rest and elevation
mark area of cellulitis
oral penicillin V and flucloxacillin
if severe may need IV abx
What is erysipelas?
infection involving the upper dermis and extends into the superficial cutaneous lymphatics
distinguished clinically by lesions raised above surrounding skin, clear line of demarcation of involved and not involved tissue
Group streptococci A most common cause
most common on legs or face
diagnosis: clinical appearance
treatment: penicillin
What is staphylococcal scalded skin syndrome?
seen in infants, young children and immunocompromised
clinical:
- starts with erythema, then fever, followed by large fluid filled bullae (large blister containing serous fluid), rupture and causes widespread exfoliation
toxins released into blood from localised S aureus infection - can die from this
Treatment: flucloxacillin
What do you worry that cellulitis might progress to?
necrotising fasciitis
What is necrotising fasciitis?
can be caused by one organism on its own (group A strept) or combination of bacteria
enter fascial plane following trauma, surgery or occult bacteraemia
inflammatory response - affects neurovascular bundles
thrombosis of vessels compromises blood supply and nerves to the skin
What are the 3 stages of symptoms in necrotising fasciitis?
1) early (<24 hours)
- presence of skin trauma but pain seems disproportionate to injury
- flu like symptoms and thirst
2) advanced symptoms
- swelling of painful area
- large dark blotches (violet)
- mottled flaky appearance at trauma site
3) critical symptoms
- severe fall in BP
- toxic shock from poisons released by bacteria
- unconsciousness
TX= IV abx and surgery
What is gas gangrene?
very rare - common cause of death in the past military conflicts - arising in devitalised wounds contaminated with soil
clostridium perfringens - most common cause - produces toxin which causes cell death
can occur in synergistic soft tissue infections e.g. wound contaminated with coliforms - use up oxygen making it amenable for anaerobes to grow
Tx= urgent surgery to remove dead tissue
Which patients is gas gangrene more common in ?
underlying blood vessel disease, diabetes or colon cancer
What are surgical site infections?
infections that affect the surgical wound or deeper tissues handled during the procedure resulting in local signs and clinical symptoms
up to 20% of all healthcare associated (nosocomial) infections - >5% of patients who undergo surgery develop an SSI
associated with morbidity, extended hospital stay and financial burden to patients and healthcare system
majority are preventable
What is the actual definition of SSI?
incisional (superficial or deep) organ/space infection - has to occur within 30 days or 1 year if an implant was inserted
Criteria
1) assessment of the surgical site (purulent drainage)
2) microbiology culture/s from sterile sites
3) signs of infection (fever, pain, tenderness, redness, heat)
What patient factors impact risk of SSI?
extremes of ages poor nutritional state obesity immunosuppression, diabetes, steroids smoking infections at other body sites
What microbial factors impact risk of SSI?
level of contamination (with prophylaxis)
clean wound 5%
clean contaminated 10%
contaminated 20%
What procedural factors impact risk of SSI?
length of surgical scrub skin anti-sepsis pre-op shaving pre-op skin prep length of op operating theatre ventilation inadequate instrument sterilisation foreign material at surgical site
What pre-op measures can be in place to prevent SSI?
patient preparation (showering)
hair removal (clippers)
antibiotic prophylaxis
staff preparation
What intra-op measures can be in place to prevent SSI?
operating team preparation
patient skin preparation
maintaining patient homeostasis
wound dressings
What post-op measures can be in place to prevent SSI?
dressing and cleaning wound
antibiotic treatment
debridement
specialist wound care services
What are the typical features of SSI?
Increased exudate increased swelling increased erythema increased pain increased local temperature peri-wound cellulitis - invasive infection, change in appearance of granulation tissue (discolouration, prone to bleed, highly friable)
What are the 2 major types of bone infections?
septic arthritis - infection of joint spaces, s. aureus, streptococci, gram negatives
osteomyelitis - infection of bone - s.aureus, h. influenzae, e.coli, p.aeruginosa, proteus mirabilis
What are the different routes by which bacteria can enter a joint in septic arthritis?
haematogenous route= most important
direct inoculation via trauma
arthritis with associated tendonitis
more common in a joint affected by rheumatoid disease or history of trauma
bacteria in an occult bacteraemia enter joint space=>inflammatory response= invasion of neutrophils into the joint
What is acute osteomyelitis?
bone may become infected following direct introduction into the tissue by trauma/surgery or by haematogenous route
chronic or acute infection
What are the clinical features of acute osteomyelitis in adults ?
severe pain reluctant to move fever, malaise backache history of UTI or urological procedure old, diabetic, immunocompromised
What are the clinical features of acute osteomyelitis in infants?
failure to thrive, drowsy, irritable
metaphyseal tenderness
decrease ROM
commonest around knee
How do you diagnose osteomyelitis?
Hx and clinical exam FBC, ESR, CRP, Blood cultures XR US Bone scan MRI Aspiration
What is the treatment for osteomyelitis?
flucloxacillin
- or clindamycin if penicillin allergic
- or vancomycin if MRSA (+ fusidic acid or rifampicin if prothesis present or life-threatening condition)
treat acute infection for 4-6 weeks
treat chronic infection for at least 12 weeks
What do diabetic foot ulcers progress from?
cellulitis> deep soft tissue infection> osteomyelitis
What are the risk factors for diabetic foot infections?
vascular disease
peripheral neuropathy
poor foot care
What organisms usually cause diabetic foot infections?
s. aureus, beta-haemolyic streptococci, diphtheroids
gram-ve bacilli (e.coli, k. pneumoniae, pseudomonas sp)
anaerobes
What viruses can cause skin reactions?
herpes and vzv (chickenpox)- can persist in dorsal root ganglia and have potential to reactivate
other viruses: rubella, parvovirus, measles, HSV6
HSV limited to genital and oral regions -
What are dermatophyte infections?
fungi invade dead tissues of the skin or its appendages (nails and hair)
most common = trichophyton, epidermophyton and microsporum
difficult to distinguish clinically
spread from person to person or animal to person
How do you diagnose dermatophyte infections?
based on site
tinea corporis = ringworm
tinea pedia = athlete’s foot
tinea barbae = barber’s itch
What is the treatment for dermatophyte infections?
topical imidazoles or other anti-fungal preparations e.g. nystatin, canestan, clotrimazole
drug resistant strains or those with invasive life-threatening infections require triazole therapy (fluconazole)
