BMFL4 Skin Soft Tissue Infections 23 NR.pptx

Leading the world to better health RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn SESSION ID: BMFML4 Skin & Soft Tissue Infections Class: Year 1 Course: Undergraduate Medicine Lecturer: Prof. Manaf AlQahtani Date: 12th November 2023 LEARNING OUTCOMES AT THE...

Leading the world to better health RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn SESSION ID: BMFML4 Skin & Soft Tissue Infections Class: Year 1 Course: Undergraduate Medicine Lecturer: Prof. Manaf AlQahtani Date: 12th November 2023 LEARNING OUTCOMES AT THE END OF THIS LECTURE YOU SHOULD BE ABLE TO…. 1. Describe the causes of skin & soft tissue infections (bacterial / viral / fungal / parasitic aetiology) 2. Recognise the clinical presentations of skin and soft tissue infections 3. Choose the most appropriate specimens for the diagnosis of skin and soft tissue infections 4. Identify which skin and soft tissue infections are life threatening & require urgent attention 5. Choose the most appropriate antimicrobials to treat patients with skin and soft tissue infections WHAT LIES ON OUR SKIN? • Resident flora – e.g. Staph. epidermidis (>90% of skin flora) – Others • Transient flora – e.g. Staph. aureus, gut flora – Colonisation vs. infection • May vary by site, e.g. hand versus groin LIFE-THREATENING BACTERIAL SKIN & SOFT TISSUE INFECTIONS 1. Cellulitis – Most cases are mild and may even be managed with oral antibiotics from home – Has potential to lead to severe sepsis if not treated appropriately 2. Necrotising fasciitis 3. Gas gangrene 1. CELLULITIS • Acute infection of skin and subcutaneous tissues • Precipitant is often a break in the skin • Pathogens: – Staphylococcus aureus – Streptococcus pyogenes (Group A beta-haemolytic streptococci) – Less commonly Group C or G beta-haemolytic streptococci CELLULITIS Clinical Features: • Erythema, swelling, pain, hot to touch • Often well-demarcated • May be evidence of precipitating skin break – Though most often not • Patient may be systemically unwell – i.e. febrile, tachycardic Risk factors: 1. Previous cellulitis 2. Diabetes mellitus 3. Obesity 4. Peripheral vascular disease 5. Lymphoedema 6. Skin breaks: – Leg ulcers – IV drug use – Trauma – Insect bites CELLULITIS - MANAGEMENT • Blood cultures, skin swab (if indicated) • Mark boundaries of cellulitis • IV antibiotics (or PO in less severe cases): – Start smart (Empiric) - flucloxacillin (covers Staph. aureus & Strep. pyogenes) but consider MRSA risk factors – Then focus (Directed) – based on culture & susceptibilities, e.g. change to benzylpenicillin if S. pyogenes confirmed) • Manage any underlying cause 2. NECROTISING FASCIITIS • Severe destructive bacterial infection of skin, subcutaneous & peri-muscular fat – With necrotic liquefaction of fatty tissue • Precipitants: minor trauma, stab wounds, surgery • Pathogens: – Type 1: Polymicrobial – Type 2: Group A beta-haemolytic streptococci (flesh-eating bug) – (Type 3: Gas gangrene) Source Unknown NECROTISING FASCIITIS Clinical Features: • SEVERE infection, rapidly progressive • Pain out of proportion to clinical appearance – Skin can initially look normal • Shiny skin / blisters • Skin colour changes as deprived of blood supply due to necrosis • Patient is systemically very unwell • HIGH mortality (20- 47%) NECROTISING FASCIITIS Source Unknown Management • Prompt diagnosis • Urgent surgical assessment & debridement of dead tissue – Send tissue for culture & susceptibility – N.B. Fresh, not in formalin • Blood cultures Antibiotics – Discuss with clinical microbiology/ID – Start smart: Broad-spectrum empiric therapy e.g. vancomycin + piperacillin-tazobactam+ clindamycin – Then focus: If group A strep, benzylpenicillin + clindamycin (suppresses toxin production) • Supportive management in ICU FOURNIER’S GANGRENE • Form of necrotising fasciitis occurring in the perineum • Full thickness necrosis of perineal skin • May involve scrotum, penis & abdominal wall • Severe & disfiguring Pathogens: Usually polymicrobial, including anaerobes Management Source Unknown • Extensive debridement vital • Broad-spectrum antibiotics 3. GAS GANGRENE (“CLOSTRIDIAL MYONECROSIS”) • Necrotising myositis • Pathogens: toxin-producing Clostridium spp. – Clostridium perfringens – C. septicum • Precipitated by: – Direct inoculation of wound (trauma or surgery) – Haematogenous – C. septicum from GIT if colon cancer Source Unknown GAS GANGRENE Clinical Features – Acute onset of severe pain – Devitalisation of limb, mottled skin – Fluid or gas-filled blisters on skin – Systemically unwell – Foul odour, crepitus Diagnosis – CT/ X-ray: Gas in tissues – Wound swab/ blister fluid/tissue for culture – Blood cultures CT showing gas gangrene (Air in thigh as well as in femoral vein) GAS GANGRENE Treatment • Surgical debridement • Antibiotic therapy – Broad-spectrum empirically – Change to benzylpenicillin when Clostridia confirmed • Supportive care in ICU • Hyperbaric oxygen CLINICAL CASE 1 • 60yo man presents to ED • Scraped his lower leg on a fence 3 days ago • Temp 38.2, otherwise well • BP 120/70, HR 90 bpm DESCRIBE THE BELOW IMAGE WHICH ONE OF THE FOLLOWING IS THE MOST LIKELY CAUSE? 1. Anaerobic streptococci 2. Staphylococcus aureus 3. Beta-haemolytic streptococci Group D 4. Clostridium perfringens 5. Staphylococcus saprophyticus WHICH ONE OF THE FOLLOWING IS THE MOST APPROPRIATE TREATMENT? 1. 2. 3. 4. Ciprofloxacin Co-amoxiclav Flucloxacillin Piperacillintazobactam 5. Vancomycin HOW WOULD YOU MONITOR THIS PATIENT’S RESPONSE TO TREATMENT? CLINICAL CASE 1 How do you assess spread of cellulitis? 1. Ask the patient about symptoms 2. Daily white cell count & CRP 3. Mark the edges & observe 4. Monitor temperature & level of pain 5. Ultrasound of the affected area (as needed) 6. Mark the edges & observe WHAT WOULD THE POTENTIAL DIAGNOSIS BE IF THIS WAS THE CLINICAL PRESENTATION? 1. 2. 3. 4. 5. Cellulitis Acute ischaemic limb Folliculitis Necrotising fasciitis Gas gangrene LESS SERIOUS BACTERIAL SKIN & SOFT TISSUE INFECTIONS 1. 2. 3. 4. 5. 6. Impetigo Folliculitis Furuncules Carbuncles Abscesses Erysipelas 7. Scalded skin syndrome (refer to Staphylococci lecture) 8. Acne 9. Bites 10.Diabetic foot infection 11.Surgical site infection Unlikely to be life-threatening, but 10 & 11 can progress to severe sepsis IMPETIGO • Infection confined to superficial skin layers • HIGHLY infectious / Outbreaks in creches Pathogens • Group A, C or G streptococci • Staphylococcus aureus Clinical • Usually exposed sites, e.g., face, arms, legs • Vesicles initially  golden crusted lesions Diagnosis • Clinical • Culture of exudate Treatment • Flucloxacillin Folliculitis Superficial infection of hair follicles & apocrine structures Pathogens • Mostly S. aureus Clinical / Diagnosis • Small pruritic papules with central pustule Treatment • Often not required • Flucloxacillin if persistent/ extensive Furuncles Deep inflammatory nodule, usually develops from preceding folliculitis • Axillae, buttocks (skin with hair follicles) Treatment • Spontaneous or surgical drainage CARBUNCLE & ABSCESSES Carbuncles: • Larger, deeper than a furuncle • Extending into subcutaneous fat • Nape of neck, back or thighs • Patient may be systemically unwell Abscesses: • An abscess is a localised collection of pus • Pathogens: S. aureus / polymicrobial • Treatment: – Incision & drainage – Usually NO role for antibiotics ERYSIPELAS • Superficial form of cellulitis with lymphatic involvement • Epidemiology: Children, elderly, diabetics • Pathogens: Mostly group A strep • Clinical/Diagnosis: – Painful erythematous lesion with elevated, well-defined border – Face or legs – May be febrile/ unwell • Treatment: – IV benzylpenicillin – PO switch to oral amoxicillin – Or oral antibiotics from outset Involved skin is raised and differentiated from uninvolved skin. ACNE • Multi-factorial skin disorder 1. Excess sebaceous secretion by follicles 2. Blocked sebaceous gland leads to pustules Pathogens: • Secondary infection with Cutibacterium spp. – Inflammation & scarring Treatment: • Broad-spectrum antibiotics e.g. doxycycline TRAUMATIC WOUNDS - CLOSTRIDIUM TETANI Tetanus is a life-threatening illness manifested by muscle rigidity & spasms caused by the spore forming organism Cl. tetani The symptoms and signs are caused by a neurotoxin (tetanospasmin) produced by the vegetative form of Cl. tetani Image: medical-labs.net Tetanus is a vaccine preventable disease Image: Merck Manuals Professional edition TETANUS, EPIDEMIOLOGY & PATHOGENESIS • Incidence varies worldwide • Wealthier countries = decreasing due to immunisation • Cl. tetani spores survive in environmental • Spores are introduced via skin trauma, often a puncture wound, burns, trivial wounds, the umbilical stump in the newborn infant – spores may contaminate heroin • Person-to-person transmission does not occur PATHOGENESIS OF TETANUS • Spores found in soil, intestines & faeces of animals; humans may harbour organism in GIT • Spores may contaminate heroin • Spores in wound germinate when there is a localized anaerobic environment (necrotic tissue) • A tiny area with relatively anaerobic conditions is required for Cl. tetani spores to germinate • Toxin blocks transmission at inhibitory synapse resulting in ‘inhibition of inhibitory neurons’ → sustained muscle contraction/spasms PRESENTATION • Muscle Spasms – May be frequent, last minutes, & persist for 3-4 weeks – Muscles of the thorax, abdomen and extremities = flexion of arms, extension of legs, arching of back – Trismus or “lockjaw” – “risus sardonicus”(sardonic appearance) produced by increased tone of orbicularis oris • Complications – Laryngospasm – Autonomic nervous system dysfunction (labile BP, arrhythmias, sweating) The mortality rate is ≥ 60% in severe cases TETANUS PREVENTION WOUND TOILET & IMMUNISATION • Prevented by immunisation with toxoid vaccines • Recovery from tetanus does confer natural immunity • The majority of cases are birth-associated among newborn babies & mothers not vaccinated • Toxoid vaccine is part of childhood vaccination programme in many countries: DTP (diphtheria-tetanus-pertussis) vaccine – Clinical efficacy almost 100% but immunity wanes & after 10 years may not provide protection ANIMAL BITES Pathogens • Animal mouth flora • Staphs / Streps Diagnosis • Send swab (or tissue if debriding) for culture & susceptibility Management • Tetanus prophylaxis • Usually co-amoxiclav – Discuss with Micro if deep infection / osteomyelitis or not resolving HUMAN BITES Pathogens • Mouth flora – e.g. strep, anaerobes Management • Tetanus booster • Antibiotics (usually co-amoxiclav) • Consider blood-borne viruses • Check for deep infection: • Is there osteomyelitis? DIABETIC FOOT INFECTIONS Limb-threatening versus non-limb-threatening Non-limb-threatening • Cellulitis, no vascular compromise, no abscess Pathogens: • Staph. aureus, βhaemolytic strep Treatment: • Flucloxacillin – Cellulitis: 5-7 days – Superficial ulcer: 5 days – Deep ulcer: flucloxacillin + metronidazole - 7 days Severe & limbthreatening • Vascular compromise / abscess / osteomyelitis / gangrene • Need radiological imaging to rule out osteomyelitis if this is suspected MANAGEMENT OF SEVERE DIABETIC FOOT INFECTIONS Involve MDT: • Endocrinology i.e. glycaemic control • Diabetes nurse specialist • Vascular surgeons re drainage/ debridement • Radiology: is there osteomyelitis? • Microbiology/ID antibiotic choice • Podiatrist • ?OPAT team if osteomyelitis ANTIBIOTIC TREATMENT OF SEVERE DIABETIC FOOT INFECTIONS • Start smart: Empiric broad-spectrum – Co-amoxiclav – Piperacillin – tazobactam (If evidence of sepsis, previous inpatient admission for diabetic foot infection, previous growth of Pseudomonas aeruginosa from foot specimen) • Broad spectrum aims to cover S. aureus & streptococci / Gram-negatives / anaerobes) – Often ulcers colonised with multiple organisms so swabs may not be helpful – Tissue or bone specimens from debridement or bone biopsy are the specimens of choice to identify the pathogen(s) • Treatment duration: approximately 10-14 days if just soft tissue / 6-12 weeks if bone involvement More in year 2 Endocrine module SURGICAL SITE INFECTIONS (SSI) • Very common healthcare-associated infection • Risk Factors – Type of procedure – Patient factors • Surgery type: – Clean (no breach of tract e.g. excision of a skin lump) – Clean- contaminated (breach of GI/ GU/ Respiratory etc. tract) – Contaminated (operating in a contaminated field e.g. post GI perforation) CLASSIFICATION OF SSI • Superficial • Deep/Incisional • Organ/Space Pathogens: • Staphylococcus aureus (most common irrespective of type of surgery) • Beta-haemolytic streptococci • Gram-negative bacilli (mostly only seen post clean-contaminated or contaminated surgery) • Anaerobes (post clean-contaminated or contaminated surgery) • Coagulase-negative staphylococci (if prosthetic material) PREVENTION OF SSI • Pre-operatively – optimise risk factors such as diabetes mellitus – MRSA decolonisation before some procedures if carriage • Intra-operatively: – No shaving, skin asepsis, choice/timing of antibiotic prophylaxis – surgical technique, theatre conditions, short duration procedure – Glycaemic control, oxygenation • Post-operatively: – Removal of drains, asepsis when reviewing wound CLINICAL CASE 2 • A 57yo male develops erythema & tenderness around his wound 4 days after bowel surgery for cancer • A superficial swab was taken on the ward SUPERFICIAL SWAB GROWS STAPHYLOCOCCUS EPIDERMIDIS – IS THIS SIGNIFICANT ? WHY? CLINICAL CASE 2 • Patient was subsequently taken to theatre for exploratory laparotomy which reveals an intra-abdominal collection of pus & samples are taken. WHAT CATEGORY OF SURGICAL SITE INFECTION (SSI) IS THIS? 1. Deep 2. Incisional 3. Organ space 4. Superficial 5. Trivial WHAT ORGANISMS ARE MOST LIKELY TO BE THE CAUSE? 1. Campylobacter spp & Shigella sonnei 2. Candida albicans & Tricophyton spp. 3. Clostridium septicum & Haemophilus spp. 4. E. coli & anaerobes 5. Staphylococcus epidermidis & Staph. saprophyticus CLINICAL CASE 3 • A 64yo gentleman with a diagnosis of Type 2 Diabetes presents to the Diabetes clinic for a routine visit • Foot exam shows the following: DESCRIBE THE IMAGE BELOW CLINICAL CASE 3 • As part of the clinic visit the patient has a superficial swab taken of the ulcer by the doctor in clinic • Swab results shows mixed growth of: – Staphylococcal epidermidis – Staphylococcal capitis DOES THIS PATIENT REQUIRE ANTIBIOTICS. WHY / WHY NOT? WOUND COLONIZATION • Superficial swabs taken from diabetic ulcers likely represent colonising flora if wound has not been appropriately cleaned and debrided • If a swab is being sent from a diabetic ulcer should be done so after cleaning and debridement of any dead skin / tissue and taken from base of ulcer • Avoid debridement if foot ischaemic CLINICAL CASE 3 • Patient presents two weeks later to the emergency department with fevers / chills / and new pain and erythema around foot ulcer site • The ulcer is now very sloughy-looking and appears to have deepened • The patient requires admission for sepsis secondary to infected deep diabetic foot ulcer WHAT IS THE MOST APPROPRIATE ANTIMICROBIAL REGIME TO COMMENCE PATIENT ON? A.Flucloxacillin B.Piperacillin – tazobactam C.Vancomycin D.Ciprofloxacin E.Benzylpenicillin VIRAL SKIN INFECTIONS • Warts • Cold sores (Covered in ‘Herpes virus’ lecture) • Hand, foot & mouth disease (Covered in ‘GI Hep module  GI viruses lecture) HUMAN PAPILLOMA VIRUS (HPV) • Genital warts - STI • Common warts – Children – Infection by direct contact – Palms, wrists, dorsum of hand – DNA virus infects epidermal cells hypertrophy & multiply leading to keratinised nodular papilloma Treatment • Childhood: self-resolution • Excision, salicylate & lactic acid ointment • Freezing, cryoprobe or liquid nitrogen FUNGAL SKIN INFECTIONS • Candida • Ringworm • Pityriasis versicolor Refer back to your lecture: Introduction to fungi and fungal infections for detail PARASITIC SKIN INFESTATIONS • Scabies • Lice SCABIES • Scabies mite (Sarcoptes scabiei) • Mite burrows into epidermis • Clinical features – Characteristic burrows in finger webs – Itch ++ (worse at night) – ‘Norwegian scabies’: diffuse crusted lesions (same parasite but in immunocompromised patients) • Highly infectious Outbreaks: Household, boarding school • Treatment – Topical permethrin- messy, need to leave on overnight – Wash clothes/ sheets etc. as well LICE (PEDICULOSIS) • Headlice (Pediculus capitis) – Common in children, outbreaks in schools, spread by direct contact – ‘Nits’ (eggs) attached to bases of hairs – Itch / papular lesions – Treatment: Malathion or 1% permethrin. Fine combing to remove nits. Bathing/ washing clothes • Body lice (Pediculus humanus) • Pubic lice (Phthirus pubis) CLINICAL CASE 4 • A 35yo nurse, who works in a nursing home, develops lesions on her fingers which are very itchy • She has no underlying skin or medical condition. WHAT ELSE WOULD YOU LIKE TO KNOW? WHAT IS THE MOST LIKELY DIAGNOSIS? 1. 2. 3. 4. 5. Abscess Acne Candidiasis Erysipelas Scabies IN ADDITION TO SPECIFIC TREATMENT, WHAT ELSE SHOULD SHE DO? 1. Apply topical steroid cream 2. Change bed clothes 3. Discontinue regular exercise 4. Eat natural yogurt twice daily 5. Take analgesia SUMMARY: SKIN AND SOFT TISSUE INFECTIONS Bacterial Viral Fungal Parasites • Necrotising fasciitis • Herpes • Candida (Infestation) • Tinea • Gas gangrene • Coxsackie Virus • Lice • Cellulitis • HPV • Pityriasis versicolor • Scabies • Abscess/Folliculitis • Erysipelas • Impetigo • Scalded skin syndrome • Animal bites • Diabetic foot SUMMARY • Skin & soft tissue infections are common but most are relatively minor • Bacterial causes are often found on the skin, e.g. Staph. aureus or the respiratory tract, e.g. Group A streptococci • Common, usually minor infections include impetigo, carbuncles & SSI (healthcare-associated) • Warts, tinea & scabies are relatively common viral, fungal & parasitic infections, respectively, requiring specific treatment YEAR 1 STUDENTS IN NEED OF ASSISTANCE • RCSI Student Assistance Programme – • RCSI Centre for Mastery: Personal, Professional & Academic Success (CoMPPAS) – – • • https://www.mercersmedicalcentre.com/rcsi-students For urgent medical advice/emergency outside regular hours contact DubDoc (Out of Hours GP) (+353) 014545607 https://www.dubdoc.ie/ – • If require urgent assistance from RCSI, or you are on campus you can contact security at 01 402 22 19. This number will not result in an in person response. Please note that in an emergency your safest action is to contact the local emergency services (112/999). If you are an International Student you should also contact your Embassy/ Sponsor to advise them of your circumstances. Mercers Medical Centre (General Practice) for health/COVID advice: – • A multidisciplinary team of RCSI professionals and specialists working collaboratively to empower students to achieve their academic, personal and professional goals: Moodle page: https://vle.rcsi.com/course/view.php?id=2583 • General Queries: [email protected] • Career Development: [email protected] • Academic Development: [email protected] • Learning Support (Disability) : [email protected] • Student Welfare : [email protected] Niteline: 1800 793 793 (Instant messaging on https://niteline.ie 9pm-2.30am every night of term). Late-night listening, support and information service run by students for students in the greater Dublin area. RCSI Security Emergency Contact (+353) 01-402219 : – • If you need urgent emotional support contact our student assistance programme available 24/7/ 365. This service provides counselling free of charge to our students: • Freephone: 1800 851 340 • International: 00353 1 518 0277 • WhatsApp: Text 'Hi' to 087 369 0010 DubDoc provides urgent medical care to patients that cannot wait to be seen by their usual GP. Emergency Services dial 999/112. The Body: Movement & Function – CASE SLIDE • The details from our class today relate to CBL Case 2