SKIN AND SOFT TISSUE

INFECTONS
INTRODUCTION
•Skin and soft tissue infection includes infection of skin,
subcutaneous tissue and fascia, and muscle .
•Staphylococcus aureus is the most common cause

EPIDEMIOLOGY:
Incidence
Annually >4million patients are seen in ED
Increases by 1 million every year from 2007
Trend correlates with greater prevalence of CA-MRSA
ANATOMY AND PATHOPHYSIOLOGY
• History
• Physical examination
• Investigations
• Surgical exploration or debridement
DIAGNOSTIC TESTINGS

• Wound cultures: only complicated purulent infection or in case of diagnostic

uncertainty, as in abscess with animal bites -gram staining

• Blood cultures: in case of deep tissue infection or systemic infection ,

multifocal infection suggesting hematogenous seeding

• Radiographic studies:

 x-rays: if foreign body suspected or evidence of osteomyelitis ( bone scan and

MRI are definitive)

 USG: foreign bodies, differentiating abscess and cellulites

 CT : reveal soft tissue gas or inflammation along fascial planes, in after

surgery or in recurrent perianal abscesses
 CELLULITIS AND ERYSIPELAS
cellulitis
• Caused by: 80% caused by communitiy acquired
methicillin-resisant staph aureus (CA-MRSA)

• Involve deeper dermis and subcutaneous tissue

• Middle age and elderly with mean age of 46 yrs

• Common sites: extremities

• Tender , warm, erythematous and swollen

• Edema – dimpling of the skin

• Recurrent episodes causes impairment of lymphatic

drainage – permanent swelling, dermal fibrosis,
Cellulitis. Note diffuse inflammation on right leg
epidermal thickening including the skin over the ankle and dorsum of the
foot
• Fever , leukocytosis, bacteremia : in
immunocompromised
Erysipelas
• Caused by beta hemolytic streptococci
• involving upper dermis
• Common among children and elderly
• Common site: face with bridge of nose
and cheeks
• Local redness, swelling and erythema
• Affected skin becomes indurated and
demarcated from surrounding normal
skin, raised border, with prominent
lymphatic involvement
• Erysipelas. Note markedly inflamed lesion with clearly
Vesicle or bulla formation
demarcated border on right cheek, across the nose to the
left cheek
General risk factors
• Lymph edema
• Skin breakdown/site of entry
• Venous insufficiency
• Leg edema
• Obesity
• Neutropenia
• Immunocompromise
• Hypogammaglobulinemia
• Chronic renal disease
• Cirrhosis
PATHOPHYSIOLOGY
• break in the normal skin integrity followed by bacterial invasion
leads to inflammatory reaction

DIAGNOSIS: Clinically

TREATMENT:
General management:
• Elevation of the affected limb

• Incision drainage of any abscess

• Antibiotics for cellulitis

• Treating underlying condtions

Empirical antibiotic treatment of purulent cellulitis
GUIDE BY SEVERITY OF
ILLNESS
mild disease: drainable
abscess with no signs of
systemic infection
Purulent cellulitis without
signs of systemic infection
Or drainable abscess with
mild to moderate signs
Purulent cellulitis with
signs of systemic infection
or drainable abscess with
mod-severe signs
ANTIBIOTICS COMMENTS
No antibiotics
Drainage od abscess
Oral: trimethoprim- Wound culture
sulfamethoxazole or Inpatient management if
doxycycline or clindamycin failed improve as
outpatient anitbiotics
IV : for MRSA coverage: Admission to Icu who meet
Vancomycin/ criteria for sepsis
Linezolid/
Daptomycin/
Clindamycin
For sepsis or unclear
etiology: piperacillin-
tazobactum or
meropenem/imipenem
Empiric treatment of non-purulent cellulitis/erysipelas

• Mild disease ( no signs of systemic infection) :oral- cephalexin

or dicloxacillin or clindamycin
• Moderate disease: IV monotheraphy- ceftriaxone or cefazolin
or clindamycin
• Severe disease: broad spectrum antibiotics: vancomycin +
piperacillin-tazobactum , or meropenem or imipenem-
cilastatin
IMPETIGO

• Superficial skin infection caused by staph aureus

• Prevalent in children 2-5years

• Communicable- person to person, autoinnoculation, fomites

• Manifested as an infection of previously intact skin or infection

damaged from minor trauma or atopic dermatits
• Rarely progesses to systemic illness

• Most cases of poststreptococcal glomerulonephritis belived to be

caused by impetigo( 10 days after onset of impetigo but upto 5weeks
later )
Clinical features and differential diagnosis

Two forms: nonbullous and bullous

Nonbullous:
• most common – group A
streptococci, staph aureus,
streptococcus pyogenes in
combination with staph aureus
• Thin walled vesicles to pustules-
rupture results in honey crusted
Classic nonbullous impetigo. Note lesions
lesions- on face or extremities with a “honey-colored” crust around the
nose and mouth.
• Bullous impetigo: staph
aureus, CA-MRSA
-Produces epidermolytic
toxin cause separation of
dermo-epidermal junction –
bullae

Bullous impetigo.
Notebullous lesion (arrow).
Ecthyma or deep impetigo:
•ulcerative form of impetigo extends
through epidermis into dermis
•Manifests as ulcers with punched-
out appearance with raised
reddened margins covered with thin Ecthyma. Note necrotic
lesion on the nose.
crusts
•Results in cutaneous scarring
Pathogens
•S. aureus and S. pyogenes are the two main pathogens.
•In neutropenic patients, a clinical syndrome termed ecthyma gangrenosum
is due to disseminated Pseudomonas aeruginosa infection.
•Its cutaneous findings are a result of hematogenous seeding of dermal
vessels with bacteria, resulting in thrombosis, ischemia, and focal skin
necrosis.

Diagnosis
•Clinically
•Culture of bullous fluid or pus when no response to standard treatment.
Treatment
•Antibacterial therapy against both S. aureus and S. pyogenes.
•Topical therapy with mupirocin
• If concern for methicillin-resistant S. aureus (MRSA) exists, clindamycin
is recommended, otherwise, cephalexin or dicloxacillin would be
appropriate.

Prevention
Handwashing and covering draining lesions
 FOLLICULITIS
Definition
• Folliculitis is a superficial infection of
the hair follicles.
Pathophysiology
• Bacteria and purulent material
accumulate in hair follicles in the
epidermal layer of the skin.
Clinical Manifestations Folliculitis. Note the multiple, small pustules on
the chin and neck.
• Folliculitis presents with pinpoint
erythema around individual hair
follicles. A small amount of purulence
may be seen.
Pathogens
•S. aureus is the most common cause of folliculitis.
•P. aeruginosa can also cause folliculitis and is associated with the use of
unchlorinated hot tubs.
•Rarely, Candida and certain dermatophytes can cause folliculitis.

Diagnosis: clinically, but if purulent material is present, it can be cultured.

Treatment
•Folliculitis often resolves on its own.
•Warm compresses or topical antibiotics - in select cases.
Prevention
•Handwashing and covering draining lesions.
•Avoid unchlorinated hot tubs.
SKIN ABSCESS (FURUNCLE & CARBUNCLE)
Definition
A skin abscess is an infection of the dermis and deeper layers of skin that
contains purulent material.
Pathophysiology
•pathogens enter a break in the skin following trauma or when they spread
from infected hair follicles.
•When a single follicle is infected and tracks down into the dermis, it is
termed a furuncle (“boil”).
•when multiple infected hair follicles coalesce-carbuncle.
•Occasionally an abscess may develop following hematogenous
dissemination.
Clinical Manifestations
•A furuncle-Central pustule surrounded by an area of erythema,
warmth, and tenderness with underlying fluctuance.
•Carbuncles - found on the nape of the neck, where a shirt collar rubs
in people with poor hygiene.
• symptoms of systemic infection- more severe disease exists
Abscess. Note localized area of
inflammation containing a
central core of yellowish pus
(arrow) on medial aspect of
foot. This lesion occurred at
the site of a sewing needle
injury.

Carbuncle. Note multiple

furuncles that have coalesced
to form a large area of
inflammatory lesion
Pathogens
•S. aureus is the most common cause of skin abscesses (> 75% of cases).
•Beta-hemolytic streptococci and gram-negative bacteria
•Occasionally Mycobacterium tuberculosis, nontuberculous mycobacteria,
and fungi such as Coccidioides, Candida, and Cryptococcus can cause
abscesses.
Diagnosis
•Gram stain and culture of purulent material obtained from the abscess
•Radiographic imaging such as USG or CT may help further define the size
and extent of an abscess.
Treatment
•The primary treatment -incision and drainage.
•In select situations, the addition of antibiotics may be beneficial.
•Antibiotics should be considered when-
-signs and symptoms of systemic infection,
-a rapidly progressive or severe infection,
-infection in a hard-to-drain area of the body,
-extremes of age,
-immunocompromised state, or
-failure to resolve with previous incision and drainage.
-When antibiotics are indicated-treat with an empiric antibiotic regimen
that has activity against MRSA.
•oral antibiotic regimens : clindamycin, trimethoprim-
sulfamethoxazole, and doxycycline .
• Empiric intravenous regimens : vancomycin and daptomycin.
•If antibiotic susceptibilities demonstrate that methicillin-
susceptible S. aureus (MSSA) is the pathogen, include
-Oral: cephalexin and dicloxacillin,
-IV: nafcillin and cefazolin
NECROTIZING SOFT TISUE INFECTION

• DEFINITION: Spectrum of illness characterized by

fulminant , extensive soft tissue necrosis, systemic
toxicity and high mortality.
• Includes:

 Necrotizing Fascitis

 Fourniers Gangrene

 Gas Gangrene
RISK FACTORS:

• Advanced age
• Diabetes mellitus
• Alcholism
• Peripheral vascular disease
• Heart disease
• Renal disease
• Hiv, cancer
• NSAID use
• Immune system imapairment
• IV drug abuse
• Decubitus ulcers
MICROBIOLOGY
TYPE MICROORGANISM ASSOCIATIONS

I Polymicrobial Diabetes, immunocompromise, PVD

Ii Monomicrobial Otherwise healthy, history of trauma or surgery

•Group A IVDU, athlete, institutionalized
streptococcus
•MRSA
III Vibrio vulnificus Marine exposure

IV Fungal inmmunocompromise
PATHOPHYSIOLOGY

Skin trauma/ internal spread

Subcutaneous tissue bacterial

invasion (fascia)

Bacterial proliferation – toxins Angiothrombotic microbial

and enzymes production invasion – skin and deep tissues
HORIZONATL PROGRESSION VERTICAL PROGRESSION

ISCHEMIA+ NECROSIS

Inflammatory mediators release.

SYSTEMIC PROGRESSION
CLINICAL FEATURES

EARLY SYMPTOMS: (within

24hours)
• Pain in the injured area
• Flu like symptoms like
fever, dizziness, weakness
• Dehydration
• Pain is disproprtionate to
injury
• Tenderness beyond rea of
erythema
• ADVANCED SYMPTOMS:
(within 3-4 days)
• Swelling and pruplish
rash
• Bliters filled with
blackish fluid
• Crepitus
• Necrotic skin with bluish,
white or dark mottled,
flaky appearance
• CRITICAL SYMPTOMS:
(within 4-5days)
• Profound septic shock
• CNS derangement
Laboratory tests
Imaging
USG

MRI CT
FINGER SWIPE TEST

• Making 2cm incision over involved tissue down to

fascia after local anesthesia, observing for normal
blood flow and inserting a gloved finger to test for
normal tissue firmness

• POSITIVE: lack of normal bleeding or friable tissue to

minimal finger pressure
TREATMENT
• IV fluids
• Broad spectrum antibiotics:
Clindamycin + ampicillin-sulbactum + vancomycin
• Pus culture , blood culture
• Electrolyte management
• Glucose control and adequate nutrition
• Oxygen and ventilatory support
• Surgical intervention: faciotomy, debridemnet and /or
amputation
• vaccum assisted dressing
• hyperbaric oxygen theraphy
• split skin grafting- once healthy granulation tissue
appears
FOURNIERS GANGRENE

DEFINITION: necrotizing fascitis of male genitalia and perineum that

can be rapidly progessing and fatal if not treated promptly

RISK FACTORS:
• Urethral strictures

• Perirectal abscesses

• Poor personal hygiene

• Diabetes

• Immunocompromised status
 Infection spreads along
dartos, scarpas, and colles
fascia
Clinical features:
• Fever
• Perineal and scrotal pain
• Cellulitis
• Eschars
• Necrosis
• Flaking skin
• crepitus
DIAGNOSIS: clinically
TREATMENT:
• Prompt drebridment of nonviable tissue
• Broad spectrum antibiotics
• Damage to external anal sphincter- colostomy to be
done
• Glucose control
• Adequate nutrition
• Testis have separate blood supply hence need not to
be removed
• Frequent dressing of tissue defect
• Skin grafting once healthy granulation tissue appear
 GAS GANGRENE
• Rapidly progressive, potentially fatal, charaterised by
widespread necrosis of muscles and subsequent soft
tissue distruction.
• Organisms: clostridium perfringens( spore forming
gram +) isolated human GIT and female genital tarct,
clostridium bifermentas, C. speticum, C. sporogens
• Exotoxin mediated
• Inadequately treated missile wounds, crushing
injuries and high voltage electrical injuries
• Risk factors: diabetes mellitus, PVD, colon cancer,
trauma or recent surgical wound
• Symptoms:
• High fever, shock
• Massive tissue distruction
• Blackening of skin.
• Severe pain around a skin of wound
• Blisters with gas bubbles form near the infected
area
• Rapidly progressive necrosis, hemolysis,
toxemia, shock, renal failure and death
• DIAGNOSIS: Clinically, culture sensitivity
• PREVENTION:
• cleaning the wound
• Avoid contaminated material
• Improve circulation
• Tetanus toxoid injection

TREATMENT:
• High risk wound give penicillin 1.5megaunits 4 hourly or tetracyclin and
metronidazole
• Debridement of dead tissues or amputated with delayed primary closure
• Hyperbaric oxygen theraphy in severe cases
Other specific skin infections
Epidemology Common pathogens Theraphy

Cat/dog bites Pasturella multocida, Amox/clav ( doxy; FQ or SXT +

capnocytophaga Cindamycin)
Human bites Mixed flora, eikenella corrodens Wound treatment
Amox/clav
Fresh water injury Aeromonas FQ: broad spectrum beta
lactams
Salt water Vibrio vulnificus FQ : ceftazidime
injury(warm)
Thorn, moss Sporothrix schenckii Potassium iodine

Meat-packing Erysipelothrix Penicillin

Cotton sorters Anthrax Penicillin

Cat scratch Bortonella Azithromycin

TOXIC SHOCK SYNDROMES
• Systemic, toxin mediated bacterial skin syndromes

• Includes:

Streptococcal toxic shock syndrome

Staphylococcal toxic shock syndrome

Staphylococcal scalded skin syndrome

PATHOPHYSIOLOGY: mediated by bacterial exotoxins- superantigens

• Diagnosis : clinical

• Treatment ; clindamycin and vancomycin

-Operative debridement of necrotizing infection

 Streptococcal toxic shock syndrome

• Severe toxin mediated syndrome , rapidly

progress to shock with multiorgan failure and
death
• Organism: streptococcus pyogenes
• Toxin : pyogenic exotoxins
• Source: necrotizing infection
• Influenza like prodromal symptoms with
nausea, vomiting, diarrhea, myalgias, chills,
high fever, hypotension, tachycardia,
• Altered mental status with confusion

• Diffuse rash in 10%

• Pain is out of proportion to physical

findings

• Most will present with shock or

develop in 4 to 6 hours

• Bacteremia is common with positive

blood cultures in 60%

• Mortality 30-80%
 Staphylococcal toxic shock syndrome
• Organism: staphylococcal aureus
• Toxin: TSS 1 , enterotoxins A, B, C
• History Of Tampon Use Or Wound Infection
• Source: nasal or wound packing, tampon, infection not
obvious
• Initially diffuse erythroderma, with exfoliation after 1-2
weeks, mucosal hyperemia, desquamation of skin of
palms and soles 7-14 days after onset
• Systemic: hypotension, shock, sometimes multiorgan
failure
• <5% mortality
Staphylococcal scalded skin syndrome
• Organism: staphylococcal aureus
• Toxin: epidermolytic toxin A or B
• Disease of infants
• Source: skin flora
• Few blisters at the site of infection to exfoliation
• Tender rash, Erythema progress to bullae and
subsequent exfoliation
• Mucosa is spared
• Systemic: Fever , irritability
• Mortality <5%
• Treatment : wound care, hydration
REFERENCES

• Tintinallis emergency medicine

comprehensive study guide
• Rosen’s emergency medicine
• Bailey and love’s short practice of surgery
• Review of medical microbiology and
immunology