Transcript PHYSICAL CHARACTERISTICS OF THE SKIN

IN THE NAME
OF THE
MOST HIGH
SKIN AND
SOFT TISSUE
INFECTIONS
PHYSICAL CHARACTERISTICS
OF THE SKIN
Mechanical barrier of stratum corneum
Relatively low PH(~5.5)
Natural antibacterial substances in the
secretions of sebaceous glands
Relative dryness of normal skin
Bacterial interference
PREDISPOSING FACTORS
 Disruption of stratum corneum
Burn and bites
abrasion
Surgery
Vascular/pressure ulcer
Underlying condition (dermatitis ,HSV, varicella)
injections
Foreign body ( IV cath. Suture )
Hair follicle : normal flora
extrinsic bacteria
PREDISPOSING FACTORS
 Reduced vascular supply
 Disruption of lymphatic or venous
drainage
 Compromised immune system
IMPETIGO
Etiology
gAS
Staphylococcus aureus (MRSA has
been reported)
gCS
rarely
gGS
Gbs (in newborn)
Epidemiology
gAS: -hot,humid,summer weather (tropical, semitropical)
-young children (2 – 5 y)
-follows skin colonization by 10d
-sporadic cases in cooler climates may
be due to contagious spread from
nasopharynx
 Highly communicable
 Related to PSGN but not ARF
S.aereus: -follow nasal colonization
Predisposing factor
Poor hygiene
Crowding
Minor trauma (scratch)
Insect bite
Preexisting skin disease(dermatitis)
Clinical manifestation
Red papule  Small vesicle pustulate 
rupture 
Thick yellow stuck-on crusts
Usual site: face(around the nose and mouth)
legs
Painless
Pruritic
Mild regional adenopathy
Minimal constitutional symptoms
Recovery without scar
Bullous impetigo
S.aureus
Newborn and younger children
10% of all cases of impetigo
Epidermal split caused by exfoliative toxin
More extensive lesions
1-2 cm bullae containing neutrophils and
organism
thin paper-like crusts
TREATMENT
Topical
mupirocin
PRP
cloxacillin 250mg qid
1st g. ceph. cephalexin 250mg qid
In the past penicillins (benzathin,oral P.V,
amoxicillin)
 in case of allergy: erythromycin
 duration : 10d
FOLLICULITIS
General considerations
Etiology: Staphylococcus.aureus
Superficial infection within hair follicles
& apocrine region
papule
small(2-5mm)
erythematous
Occasionally pruritic
Topped by a central pustule
Treatment
Local measures
saline compress
topical antibacterials
Duration :until resolution of infection
(5-7 d)
Chronic folliculitis:
 Uncommon except in acne vulgaris,
 Constituents of the normal flora (e.g.,
Propionibacterium acnes) may play a
role
Diffuse folliculitis:
 Hot-tub folliculitis
 Swimmer’s itch
Hot-tub folliculitis
Pseudomona.aeruginosa:
-contaminated swimming pools
insufficiently chlorinated , 37-40°c
-IP:48h
-papulourticarialpustule
-healing within 5 days
-bacteremia has been reported
swimmer’s itch
Exposure of skin to freshwater infested
with avian schistosomes
Warm water and alkaline PH:
suitable for mollusks(intermediate host)
Schistosomal cercariae penetrate hair
follicles but quickly dies
Allergic reaction : intense itching and
erythema
Other less common forms
Enterbacteriaceae
-complicate acne
-during prolonged AB therapy
Candida
-surrounding areas of intertriginous
-pruritic satellite lesion
-prolonged AB or C.S
FURUNCLE&CARBUNCLE
Furuncle
Deep seated (subcut.) necrotic infection
Extend from a hair follicle to a true abscess
Site:areas that are subject to friction and
perspiration and contain hair follicles
(buttock,face,neck)
Painful , firm, red nodule
Fever and constitutional symptoms
Subside after spontaneous drainage
Carbuncle
Deep infection of a group of contiguous
follicles
Site: back of the neck,shoulders,hip,thigh
More severe,necrotic and painful
External drainage along hair follicules
Intense inflammation of surrounding and
underlying connective tissue
Fever ,malaise and leukocytosis
Predisposing factors
Diabetes mellitus
Obesity
Blood dyscrasia
Corticosteroid therapy
Defect in neutrophil function
Complication
Blood stream invasion
Infective endocarditis
Metastatic foci
Osteomyelitis
Upper lip,nose: spread to cavernous
sinus
Treatment
Systemic antibiotics esp. if
cellulitis
fever
midface
Severe infection: nafcillin/cloxacillin
1-2g iv q4h
cefazolin 1g iv q8h
Mild infection:
cloxacillin/cephalexin
250-500mg po qid
Duration : 7-10d
Surgery: large and fluctuent
Furuncle
Furuncle
Carbuncle
ERYSIPELAS
Etiology
gAStrep
Uncommonly gC & gGStrep
In newborns gBStrep
Clinical manifestation
Site: formerly face was most common
now distribution has changed:
70-80%
lower extremity
5-20%
face
Infants and elderly adults most affected
Clinical manifestation
Abrupt onset
Rapid progression
 Translocation of strep. laterally via lymphatics
Flaccid edema of the epidermis
 Engorgement or obstruction of lymphatics
Clinical manifestation
Bright,red swelling
Warm , intense pain
Raised,indurated,sharply demarcated
margin
Peau d ‘ orange texture
involvement of superficial lymphatic
Flaccid bullae during 2nd or 3rd day
Desquamation 5-10 days in to the illness
Fever , leukocytosis is a feature
Extension to deeper soft tissue is rare
Treatment
Mild,early:
-procaine penicillin 1.2mu bid IM
-penicillin.V
oral
-erythromycin in case of allergy
Severe :
-penicillin.G 1-2mu q4h IV
If cellulitis is a D.Dx: -PRP(nafcillin,oxacillin)
-1st g. ceph.
Treatment
Swelling may progress despite appropriate
treatment
Fever
Pain
Intense red color
diminish
CELLULITIS
Etiology
S.aereus:
 MRSA is rapidly replacing MSSA
gA strep.
gC strep sometimes
gG strep sometimes
Wide variety of exogenous bacteria
Predisposing factor
S.aureus : central localized infection
(e.g. abscess , folliculitis , infected foreign
body , surgical or traumatic wounds)
Strep. : minor or inapparent breaks
disrupted lymphatic drainage
surgical wound infection (1st 24 h )
Clinical manifestation
Pain and local tenderness
Hot
swollen
Erythema
Strep : more rapidly spreading
frequently associated with fever
and lymphangitis
Clinical manifestation
Diffuse spreading infection
Involves skin and subcutaneous tissue
(deeper than erysipelas)
Systemic signs (fever,malaise,chills)
Regional lymphadenopathy
Border not elevated ,not demarcated
Diagnosis
If : drainage
an open wound
an obvious port of entry
gram stain
culture
In the absence of these findings definite
diagnosis of etiology is difficult
Culture of needle aspiration and punch
biopsy 20%
Blood culture <5%
Differential diagnosis
Necrotizing fasciitis
Insect bite
Fixed drug eruption
DVT
FMF
Pyoderma gangrenosa
Sweet’s syndrome
Treatment
Indications for admission:
- rapid progression
- systemic reaction (chills and fever)
- underlying condition
(immunedefficiency, asplenia, previous
edema, cirrhosis, renal failure, heart
failure)
Treatment
 Hospitalized patients:
-Nafcillin or oxacillin
-Cefazolin
2g iv
1-2g iv
q4-6h
q8h
 Mild infection
-Cloxacillin
-Cephalexin
500mg po q6h
500mg po q6h
Other agents: vancomycin, clindamycin,
erythromycin, TMP/SMX, quinolones (CAMRSA)
Treatment
Duration : 10-14 days
Shift from IV to PO after systemic symptoms
and erythema resolved
Recurrent forms
 Saphenous venectomy for CABG
Edema,erythema,tenderness
Chills,high fever,toxicity
Associated lymphangitis
Spread along the course of venectomy
Etiology:gA & non gAßHS (gC,gG)
Port of entry:associated area of tinea pedis
Recurrent forms
Chronic lower extremity lymphedema
Radiation therapy
Neoplastic involvement of pelvic lymph
node
Lymph node dissection
Chronic venous stasis (prior DVT)
Recurrent forms
Stapylococcus :
 Job ‘s syndrome (eosinophilia and, IgE)
 Nasal carriers of staph
Other microorganisms
S.agalactiae(gBS)
 Elderly, diabetes, neurologic impairment,
Peripheral vascular disease, HIV
Haemophilus.influenza
 Children
 Violaceous, facial cellulitis(periorbital,cheek)
 In association with sinusitis,otitis,epiglotitis
Other microorganisms
P.aeruginosa
 3 types of soft tissue infections:
 Ecthyma gangrenosum in neutropenic patients
 Hot tub folliculitis
 Cellulitis : penetrating injuries (step on a nail)
hospitalized immunocompromised host
Treatment :surgical drainage and inspection
+ antimicrobial (AG , 3rd generation ceph.
, semisynthetic penicillin , quinolone)
Other microorganisms
Pasteurella multocida, Staphylococcus
intermedius and Capnocytophaga
canimorsus
cat or dog bite
Eikenella corrodens
human bite
Amoxicillin/clavulanate, ampicillin/sulbactam,
and cefoxitin are good choices for the treatment
of animal or human bite infections
Other microorganisms
Erysipelothrix.rhusiopathiae
Fish and domestic swine: butcher, fisherman, veterinarian
Aeromonas hydrophilia
Fresh water (lakes,rivers,streams)
Vibrio vulnificus
Seawater or seafoods
M. marinum
water in aquariums or swimming pools
NECROTIZING SOFT
TISSUE
INFECTIONS
Necrotizing fasciitis
Destruction of subcutaneous tissue and
fascia
Physical findings ,particularly early in
the illness, may not be striking when
pain or unexplained fever is the only
manifestation with no or minimal
erythema
Infectious disease emergency
In the initial phase distinguishing between
cellulitis and fasciitis is difficult
Necrotizing fasciitis
 Involvement of deeper tissue is suggested:
 Failure to respond to therapy
 Hard , wooden feel of subcutaneous tissue
 Systemic toxicity
 Bullous lesion
 Skin necrosis and ecchymosis
 Rapid spread
 Gas in soft tissue
 Edema that extends beyond the margin of erythema
 Skin anesthesia
Necrotizing fasciitis
 Clinical manifestation :
severe local painanesthesia
cellulitis with progressive edema,erythema
dark red induration of epidermis
bullae filled with blue or purple fluid
friable skin with bluish ,maroon or black color
thrombose of blood vessels in dermal papilla
crepitation
fever , systemic toxicity shock and multiorgan
failure
Necrotizing fasciitis
TYPE 1 :polymicrobial (anaerobe,g+ ,g- )
Predisposing :- a breach in the integrity of
mucous membrane (GI or GU) : malignancy ,
diverticulum …, urethral tear
- surgery
- diabetes
- peripheral vascular disease
- injection drug use
Necrotizing fasciitis
TYPE 2 :gAstrep (streptococcal gangrene)
Predisposing :
- non penetrating minor trauma(a bruise,
muscle strain) via transient bactremia
- cutaneous infection , penetrating trauma
Toxicity is severe
20-40% myositis occur concomitantly
Markedly elevated CPK
Gas is not usually present
Fournier’s gangrene
A type of necrotizing fasciitis
Leakage to the perineal area
Mixed aerobe-anaerobe infection
Massive swelling of scrotum and penis
Extension to the prineum , abdominal wall
and legs
Necrotizing fasciitis
 Diagnosis :
Vigilant and serial clinical examination
Soft tissue radiographs and CTscans:
Local abscess or gas
only soft tissue swelling in some cases
Aspiration of the leading edge or punch biopsy:
false negative in nearly 80%
Open surgical inspection with debridement
Necrotizing fasciitis
Rx : surgical drainage and debridement:
1) visualize the deep structure
2)remove necrotic tissue
3)reduce compartment pressure
4)obtain material for smear & culture
 Hyperbaric oxygen
Necrotizing fasciitis
Rx : type 1
Ampicillin or ampicillin/sulbactam+
Gentamicin+
metronidazole/clindamycin
ampicillin +
ciprofluxacin+
metronidazole/clindamycin
type 2
penicillin G +
clindamycin
Clostridial gas gangrene
(clostridial myonecrosis)
Etiology
Clostridial spp.
C.perfringes 80 % of cases
-trauma
need not to be severe
but must be deep&necrotic
-surgery
-intramuscular injection
Etiology
C.septicumspontanous,nontraumatic
GI abn (cancer,surgery,diverticulitis)
leukemia,lymphoma
neutropenia
HIV infection
Clinical manifestation
Short IP almost always<3d frequently<24h
Sudden onset of exquisite increasing pain
Local swelling and edema
Thin hemorrhagic exudate
Frothiness of wound exudate
Tachycardia ,minor elevation in temperature
Gas may be absent at early stages
Clinical manifestation
Skin is tense , white marbled with blue and
cooler than normal
Rapid progression of edema & toxemia
Profuse serosanginous discharge with
sweetish smell
Bullae ,patches of cutaneous gangrene,
bronze discoloration
Gas in affected tissue
Clinical manifestation
High LOC until just before death
Hypotension ,renal failure
At surgery -muscle may appear pale
-does not contract
-beefy red and nonviable when
dissected
Diagnosis & Treatment
Gram stain :gram positive bacilli (box car)
paucity of PMN
Surgery: muscles are pale ,nonviable
frozen section
Rx: surgical removal of devitalized tissue
antibiotic : clindamycin + penicillin
metronidazole
chloramphenicol
hyperbaric oxygen
DIABETIC FOOT ULCERS
Chronic foot infections in patients with D.M
are common and difficult problems
Minor trauma in presence of
peripheral neuropathy , neuropathic
ulcers , vascular insufficiency
Different forms : cellulitis , tissue
necrosis , osteomyelitis
Clinical manifestation
Non limb threatening
Superficial
Lack of systemic toxicity
Minimal cellulitis < 2 cm from port of
entry
Ulceration (if present) not fully
extending through the skin
Lack of significant ischemia
Clinical manifestation
Limb threatening :
More extensive cellulitis
Lymphangitis
Ulcer penetrating through skin in to
subcutaneous tissue
Prominent ischemia
Etiology
 Non limb threatening :
S.aureus is major pathogen
Facultative streptococci in one third
Facultative gram negative and anaerobe
are uncommon
 Limb threatening :
Polymicrobial (S.aureus ,Gbstrep.
,facultative gram negative ,anaerobe)
Medical Treatment
 Non limb threatening :
Mild : oral cephalexin , cloxacillin ,
clindamycin
Complicated by cellulitis :parentral cephazolin
 Limb threatening :
Broad spectrum : eg clindamycin+3rd g ceph.
clindamycin+ciprofluxacin
Ampicillin-sulbactam
Surgical management
Unroofing
Probing
Debridement and drainage promptly if :
-deep ulcers extending to subcutan.
-deep tissue necrosis
-suppuration
Amputation
Other measures
Bed rest
Elevation
Control of diabetes
Prevention
Tight glycemic control
Examination of the foot
Avoid extreme bath water temperature
Avoid foot soaks
Dry the foot thoroughly after bath
Trim the nails correctly
Treat tinea pedis promptly
Selection of appropriate footwear