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year 4 CDM 2 > Case 12: skin infections > Flashcards

Case 12: skin infections Flashcards

1
Q

When are you most likely to suspect a brain abscess

A

In risk factors such as immunosuppression, recent neurosurgery, chronic ear or sinus infections, or systemic infection in combination with new neurological symptoms.

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2
Q

Brain abscess clinical features

A
  • Headache: dull, constant and progressively worsening
  • Focal neurological deficits: hemiparesis, language or speech disorders (aphasia, dysarthria), visual field defects
  • Fever: with chills and night sweats
  • Non-specific: lethargy, altered mental state, seizures
  • Signs of raised intracranial pressure: nausea, vomiting, altered consciousness, papilloedema
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3
Q

Brain abscess investigations

A
  • MRI with gadolonium contrast
  • Lumbar puncture: contraindicated
  • Stereotactoc needle aspiration: aids diagnosis and serve as treatment
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4
Q

Brain abscess management

A
  • Surgery: a craniotomy is performed and the abscess cavity debrided. The abscess may reform. Can trial antibiotics alone if abscess smaller than 2cm
  • IV antibiotics: IV 3rd-generation cephalosporin (ceftriaxone) + metronidazole for 6-8 weeks
  • Intracranial pressure management: e.g. dexamethasone
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5
Q

Categories of causes of a brain abscess

A
  • direct inoculation: penetrating trauma, neurosurgery
  • contiguous spread: mastoiditis, sinusitis, dental infection
  • haematogenous spread: endocarditis, IVDU

Most common causative agents of brain abscess: staph and strep

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6
Q

Types of skin and soft tissue infections

A

Cellulitis, Impetigo, Animal bites, Necrotising Fasciitis, Diabetic foot, Surgical site infection, Folliculitis and Varicella Zoster.

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7
Q

Cellulitis

A

Bacterial infection that affects the dermis and the deeper subcutaneous tissue. Commonly caused by Streptococcus pyogenes or less commonly S.aureus.

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8
Q

Cellulitis: clinical features

A
  • Commonly occurs on the shins- usually unilateral, bilateral is rare and suggests an alternative diagnosis
  • Erythema: with well defined margins
  • Swelling
  • May surround an area of trauma
  • Systemic upset: fever, malaise, nausea, lymphadenopathy
  • What might precipitate cellulitis: trauma, ulcer, bite
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9
Q

Eron classification of Cellulitis (1 and 2)

A
  • I: no signs of systemic toxicity and the person has no uncontrolled co-morbidities
  • II: systemically unwell or systemically well but with a co-morbidity (i.e. PAD, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection
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10
Q

Eron classification of cellulitis (3 and 4)

A
  • III: significant systemic upset such as acute confusion, tachycardia, hypotension, or unstable co-morbidities that may interfere with treatment, or a limb-threatening infection due to vascular compromise
  • IV: sepsis syndrome or a severe life-threatening infection such as necrotizing fasciitis
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11
Q

Cellulitis: when to admit for IV antibiotics

A
  • Has Eron Class III or Class IV cellulitis.
  • Eron II: admission may be necessary if no expertise
  • Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
  • Is very young (under 1 year of age) or frail.
  • Is immunocompromized.
  • Has significant lymphoedema.
  • Has facial cellulitis (unless very mild) or periorbital cellulitis.
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12
Q

Cellulitis investigations

A
  • Bloods: FBC, U&E, CRP/ESR
  • Wound swab: only if open wound
  • Blood culture
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13
Q

Eron class 1 and 2 treatment

A
  • oral flucloxacillin for mild/moderate cellulitis 5-7 days, IV for severe
  • oral clarithromycin, erythromycin (in pregnancy) or doxycycline is recommended in patients allergic to penicillin.
  • IV alternatives Teicoplanin, Clindamycin

Eron class II: can be managed in the community if able to give IV antibiotics (IV flucloxacillin) and monitor the person

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14
Q

Treatment for Eron class 3-4

A
  • admit
  • NICE recommend: oral/IV co-amoxiclav, oral/IV clindamycin, IV cefuroxime or IV ceftriaxone
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15
Q

General management for Cellulitis

A
  • mark the area of erythema to detect spreading cellulitis
  • if possible elevate the leg
  • consider paracetamol or ibuprofen for pain orfever
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16
Q

Complications of cellulitis

A
  • Acute infection: sepsis, subcutaneous abscess formation, myositis, fascitis, death
  • After infection: recurrence or chronic limb oedema
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17
Q

Folliculitis

A
  • An infection from a single hair follicle
  • Commonly caused by S.aureus
  • Bacterial folliculitis is prone to occur in areas of the skin subject to rubbing, occlusion, and sweating, such as the neck, face, axillae, and buttocks.
  • Presents as itchy pustules
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18
Q

Management of Folliculitis

A

May resolve spontaneously if superficial. Topical antibiotics i.e. mupirocin or oral

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19
Q

Types of folliculitis

A
  • Bacterial folliculitis: most common type
  • Hot tub folliculitis: red spots on the trunk. Pseudomonas aeruginosafrom improperly sanitised hot tubs or spas
  • Gram negative folliculitis: Rare pustular facial eruption, usually following antibiotic treatment of acne. Caused by Klebsiella, Enterobacter
  • Sycosis Barbae – distinctive form of deep folliculitis, often chronic, that occurs in beards. Often fungal in nature (candida and trichophyton)
  • Mechanical folliculitis: due to shaving
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20
Q

Impetigo

A

Superficial infection of the epidermis, caused by either staphylococcus aureus or Streptococcus pyogenes. It can be a primary infection or a complication of an existing skin condition such as eczema, scabies or insect bites. Common in children especially in warm weather

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21
Q

Impetigo pathophysiology

A

Spread is by direct contact with the scabs of an infected person. Infection is spread mainly by the hands, but indirect spread via toys may occur. The incubation period is between 4 to 10 days. Most commonly located on the face. Causes pustules that rupture leaving yellow-brown plaques and regional lymphadenopathy.

22
Q

Non-bullous and Bullous Impetigo

A
  • Non-bullous impetigo: typically around nose or mouth, exudate from lesions form a golden crust
  • Bullous impetigo: Caused by S.aureus, results in fluid filled vesicles forming which burst to form a golden crust. Heal without scarring, lesions are painful and itchy
23
Q

Bullous Impetigo

A
  • More common in children <2.
  • Tend to have systemic symptoms.
  • In severe infections where the lesions are widespread its called staphylococcus scalded skin syndrome
  • Swabs to confirm diagnosis
  • Treated with flucloxacillin either oral or IV
  • Very contagious, patients should be isolated
24
Q

Impetigo clinical features

A
  • ‘golden’, crusted skin lesions typically found around the mouth
  • very contagious
  • Tends to occur on the face, flexures and limbs not covered by clothing
25
Q

Impetigo management

A
  • First line: hydrogen peroxide 1% cream (localised non-bullous impetigo)
  • Second line: Topical antibiotic cream (topical fusidic acid if resistant topical mupirocin)
  • Extensive disease: oral flucloxacillin or oral arythromycin if penicillin allergic
  • May need to de-colonise
  • School exclusion: children should be excluded from school until the lesions are crusted and healed or 48 hours after commencing antibiotic treatment
26
Q

Impetigo complications

A
  • Cellulitis if the infection gets deeper in the skin
  • Sepsis
  • Scarring
  • Post streptococcal glomerulonephritis
  • Staphylococcus scalded skin syndrome
  • Scarlet fever
27
Q

Animal bites

A
  • Animal mouth flora eg. Pasteurella, Capnocytophaga as well as usual skin pathogens
  • Consider if rabies prophylaxis required
  • May require debridement and washout especially if deep wounds
  • Appropriate Abx: Co-amoxiclav
28
Q

Human bites

A

In case of human bites, often from a punch colliding with teeth

  • Consider risk of BBVs including HIV and Hepatitis B
  • Consider mouth flora as well as usual skin pathogens
29
Q

Necrotising fasciitis

A
  • Severe soft tissue infection causing necrosis of the subcutaneous tissue and fascia sometimes affecting the muscle
  • Typically occurs after trauma: external injuries or surgical wounds
  • Can develop in the limbs, the perineum, and genitals (also known as Fournier’s gangrene) or in the abdominal wall.
  • Pathogen: Group A Streptococci, Enterobacteriaceae
30
Q

Risk factors for Necrotising fasciitis

A
  • Diabetes mellitus (increased prevalence)
  • CKD (increased mortality)
  • Comorbidities: Cirrhosis, chronic heart failure, obesity, alcohol, SLE
  • Immunodeficidency
31
Q

Necrotising fasciitis categories (1 and2)

A
  • Type I -Polymicrobial by multiple anaerobic species, particularly affecting those with multiple comorbidities. Majority of NF and effects the trunk or perineum. Streptococci (not group A) or Enterobacteriaceae (E.coli, Klebsiella)
  • Type II - Monomicrobial, caused byStreptococcus pyogenes (alone or with other species. Occurs in younger patients and affects the limbs.
32
Q

Necrotising fasciitis (3 and 4)

A
  • Type III - Monomicrobial, caused by theClostridiumspecies most commonly and theVibriosspecies. Most frequently found in intravenous drug users.
  • Type IV - Fungal NF, mainlyCandidaspecies. Mainly found in immunocompromised patients, aggressive and extensive.
33
Q

Progression of symptoms in necrotising fasciitis

A
  • Early: swelling, pain, erythema, induration
  • Characterised by severe pain which subsides with the destruction of nerve endings, often outside margin of erythema
34
Q

Clinical features of necrotising fasciitis

A
  • Rapidly expanding inflamed area of skin
  • Blistering and bullae formation: Bullae contain serous fluid early on but may become haemorrhagic
  • Failure to respond to broad-spectrum antibiotics
  • Grey, dusky skin indicating necrosis
  • Skin crepitus: Air under the skin that causes a crackling feel when touched
  • Diarrhoea and vomiting
  • Systemic features: tachycardia, fever, hypotension and tachypnoea
  • Signs of sepsis and organ dysfunction including altered mental status
35
Q

Necrotising fasciitis investigations

A
  • The scoring system: Laboratory Risk Indicator for Necrotising Fasciitis(LRINEC): <5 is low risk, 6-7 indeterminate risk, >8 high risk
  • Wound culture, to improve antibiotic sensitivity
  • Plain x-rays, which can demonstrate subcutaneous gas
  • CT and MRI imaging: asymmetrical fascial thickening with fluid collection and gas tracking along the fascial planes. These findings have a high sensitivity
  • Incisional biopsy: showing necrosis, microorganisms, polymorphonuclear infiltration.
  • Bloods: FBC, raised CK and lactate
36
Q

Management of Necrotising fasciitis

A
  • Surgical debridement: including fasciotomy
  • Cultures
  • Multi-discipline approach in a secondary care centre
  • Antibiotics: broad spectrum antibiotics which might include Iv Flucloxacillin, IV Benzylpenicillin, IV Metronidazole, IV Clindamycin, IV Gentamicin
37
Q

Diabetic foot ulcers

A
  • Skin, soft tissue or bone infection in a foot/ankle of a patient with diabetes
  • Can lead to life-threatening infection or amputations
  • Diabetic foot ulcers act as a portal of entry for bacterial infection: Staphylococci, streptococci, pseudomonas, other gram negatives, anaerobes
  • Microbiological sampling extremely helpful
38
Q

Management: Diabetic foot ulcers

A
  • Debridement
  • Antibiotics- guided by current and previous microbiological samples
  • Supportive measures eg. weight off-loading, wound care
  • MDT approach
  • Can require amputation if gangrene, irreversible osteomyelitis, deep infection
39
Q

Surgical site infection

A

Infection at the site of previous surgery. Can be superficial skin infection or involve the deeper tissues, organs or implanted material.

40
Q

Prevention of surgical site infection

A
  • Decolonisation prior to the procedure (see local guidelines)
  • Antibiotic prophylaxis
  • Skin decontamination and surgical techniques
  • Dressing and wound care
41
Q

Management of surgical site infections

A
  • Appropriate antibiotics for site and procedure (eg. neurosurgical will be different to abdominal)
  • Debridement/drainage of any collections
  • Microbiological sampling can be helpful especially if deep infection (get deep samples)
42
Q

Orbital cellulitis

A

Affects the fat and muscle posterior to the orbital septum, within the orbit but not involving the globe. Caused by spreading URTI. Medical emergency requiring senior review.

43
Q

Risk factors for orbital cellulitis

A
  • Childhood
  • Previous sinus infection
  • Lack ofHaemophilus influenzaetype b (Hib) vaccination
  • Recent eyelid infection/ insect bite on eyelid (Peri-orbital cellulitis)
  • Ear or facial infection
44
Q

Orbital cellulitis ‘5 P’s’

A
  • Pain: throbbing or deep ache. worsens with eye movement
  • Proptosis (Exophthalmos): forward displacement or protrusion of the eyeball due to inflammation of the orbit
  • Periocular swelling (oedema): due to the inflammatory response within the orbital tissue presents with swollen eyelids, chemosis (swelling of conjunctiva) and erythema
  • Pupil involvement and visual changes: blurred vision, decreased visual acuity, diplopia (double vision) or visual loss
  • Palsy (opthalmoplegia): impaired eye movement
45
Q

Investigations and findings for orbital cellulitis

A
  • Full blood count – WBC elevated, raised inflammatory markers.
  • Clinical examination – Decreased vision, afferent pupillary defect,proptosis, dysmotility, oedema, erythema.
  • CT with contrast – Inflammation of the orbital tissues deep to the septum, sinusitis.
  • Blood culture and microbiological swab. Most common bacterial causes –Streptococcus,Staphylococcus aureus,Haemophilus influenzae B.
46
Q

Management of orbital cellulitis

A

Admission to hospital for IV antibiotics (Ceftriaxone). Surgery might be needed (orbital decompression and abscess drainage).

47
Q

Periorbital cellulitis

A

A less serious superficial infection anterior to the orbital septum, resulting from a superficial tissue injury (chalazion, insect bite etc…). Infection of the periorbital skin and soft tissue. Infection of the eyelid (superficial) Management is with oral co-amoxiclav.

48
Q

Varicella zoster (shingles)

A
  • Localised, painful blistering rash: usually maculopapular then vesicular
  • Beware ocular, disseminated and CNS disease
  • Reactivation of Varicella zoster virus (VZV).
  • Dermatomal distribution
  • More common in adults esp older people and immunosuppressed
  • After primary infection, VZV stays dormant in dorsal root ganglia nerve cells in spine for years before reactivation. It then migrates down sensory nerves to skin causing zoster.
  • Pain usually first symptom, within 1-3 days blistering rash appears in painful area of skin
49
Q

Treatment of shingles

A
  • Analgesia: NSAID’s if moderate-severe add Amitriptyline, Gabapentin etc. Use Calamine lotion
  • Antivirals within 72 hours of rash onset if: Immunocompromised, non-truncal rash involvement, moderate-severe pain or rash. Choice of oral Acyclovir, famciclovir
  • Consider anti-viral’s >50
  • Corticosteroids: consider if on anti-virals, used in the first 2 weeks after rash onset
50
Q

Post-herpetic neuralgia

A
  • The most common complication of shingles: Persistent pain in region of rash, after rash and acute illness is resolved (lasting >1 month)
  • Offer neuropathic pain killer

year 4 CDM 2 (39 decks)

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