SSSS, ECTHYMA, CELLULITIS, ERYSIPELAS.ppt

Introduction to Dermatology Summary Slides

1. SSSS, ECTHYMA, CELLULITIS,
ERYSIPELAS
ARLENE KACHAPIRA

2. Outline
•Introduction
•Pathophysiology
•Management
•Differential diagnosis
•Complication
•Prognosis

3. Staphylococcal scalded skin syndrome
SSSS
•Also known as Ritter von Ritterschein disease
(in newborns), Ritter disease, and
staphylococcal epidermal necrolysis
•Encompasses a spectrum of superficial
blistering skin disorders caused by the
exfoliative toxins of some strains of
Staphylococcus aureus

4. •It is a syndrome of acute exfoliation of the
skin typically following an erythematous
cellulitis.
•Severity varies from a few blisters localized to
the site of infection to a severe exfoliation
affecting almost the entire body.

5. Pathophysiology
•SSSS is caused by an exfoliative toxin produced
by roughly 5% of Staphylococcus aureus.
•Epidermolytic toxins are produced by the
infecting Staphylococcus species;
•These toxins act at a remote site leading to a red rash
and separation of the epidermis beneath the granular
cell layer.
•Bullae form, and diffuse sheet like desquamation occurs

6. •Two exfoliative toxins (ETA and ETB) have
been isolated
•Exact mechanism by which they cause
exfoliation had until recently been uncertain.
•The toxins likely act as proteases that target
the protein desmoglein-1 (DG-1),
•an important keratinocyte cell-to-cell attachment
protein found only in the superficial epidermis.

7. •Two types of staphylococcal scalded skin
syndrome are thought to exist:
•A localized form, in which there is only patchy
involvement of the epidermis, involving most
the skin folds
•A generalized form, in which significant areas
of are involved, remote from the initial site of
infection.

8. Presentation
•SSSS presents as a macular erythema followed by
diffuse epidermal exfoliation.
•A prodromal localized S aureus infection of the
skin, throat, nose, mouth, umbilicus, or GI tract
occurs.
•The patients my complain of:
•General malaise
•Fever
•Irritability
•Skin tenderness

9. •Diffuse erythematous rash often begins
centrally, is sandpaper like (progressing into a
wrinkled appearance, and accentuated in
flexor creases
•If Bullae present are often flaccid and ill
defined
•Exfoliation of skin, which may be patchy or
sheet like

11. •There is increased frequency of staphylococcal
scalded skin syndrome in children younger
than 5 years.
•It is theorized that immature renal function in this age
group may contribute to impaired clearance of
circulating exotoxins, contributing to more extensive
disease.
•Another theory suggests that the exfoliative
toxins may possess a superantigenic activity.

12. Management
•Workup
•WBC
•ESR
•Electrolyte
•Renal function
•Gram stain***
•CXR to r/o pneumonia
•Biopsy separation at the granular layer

13. Treatment
•The goal is to stabilize the patient condition
•Supportive care
•Fluid rehydration,
•Topical wound care similar to the care for thermal burns
•Eradication of the primary infection.
•Parenteral antibiotics to cover S aureus.
•Most staphylococcal infections implicated in staphylococcal
scalded skin syndrome have penicillinases and are resistant
to penicillin.
 
•Penicillinase-resistant synthetic penicillins (nafcillin or
oxacillin) are said to be effective

14. •Other effective drugs are
•Amoxicillin and clavulanate (Augmentin)
•Indicated for skin and skin-structure infections caused by
beta-lactamase-producing strains of S aureus. In children >3
mo,
•Cefazolin,
•First-generation semisynthetic cephalosporin, which, by
binding to one or more penicillin-binding proteins, arrests
bacterial cell wall synthesis and inhibits bacterial growth.
Primarily active against skin flora, including S aureus.
•Clindamycin
•Lincosamide useful as treatment against serious skin and
soft-tissue infections caused by most staphylococci strains.

15. •Erythromycin
•Indicated for treatment of infections caused by susceptible
strains including S aureus. inhibits bacterial growth.
•Antibacterials, Topical
•Mupirocin (Bactroban, Bactroban Nasal)
•They are Bactericidal; inhibits protein synthesis in
susceptible bacteria
•These agents are used to treat open excoriations and
erosions and can be used as adjuncts to parenteral
antibiotics, but they should not be used alone in true cases
of staphylococcal scalded skin syndrome.

16. •Avoid
•Steroids - may worsen immune function.
•Nonsteroidal anti-inflammatory agents and
other agents that potentially reduce renal
function should be avoided

17. DDX
•bullous impetigo
•Both are blistering skin diseases caused by staphylococcal
exfoliative toxin. However, in bullous impetigo, the
exfoliative toxins are restricted to the area of infection, and
bacteria can be cultured from the blister contents.
•toxic epidermal necrolysis (TEN),
But the cleavage site in SSSS is intraepidermal, as opposed to TEN,
which involves necrosis of the full epidermal layer (at the level of the
basement membrane).
•Chemical burn
•Cellulitis
•Exfoliative dermatitis

18. Complications
•Dehydration
•Shock
•Hypothermia
•Generalized bacteremia and/or sepsis
•Local or remote spread of infection
•Secondary infections
•Scarring, disability, and death

19. Prognosis
•Prognosis in children is excellent, with complete
healing typically occurring in 10 days without
significant scarring.
•Prognosis in adults depends on the host's
immune status, the speed in initiating proper
treatment, the course of the infection, and the
occurrence of complications.
•Staphylococcal scalded skin syndrome in adults
carries significant rates of morbidity and
mortality.

20. ECTHYMA

21. •Ecthyma is a skin infection characterized by
crusted sores beneath which ulcers form.
•an ulcerative pyoderma of the skin caused by group A beta-
hemolytic streptococci
•It is a deep form of impetigo as the same bacteria
causing the infection are involved but ecthyma
causes deeper erosions of the skin.
•It is often called deep impetigo because it occurs
deep inside the skin.
•Predilection for children and elderly individuals.

22. Pathophysiology
•Group A beta-hemolytic streptococci is often
implicated
•may initiate the lesion or
•may secondarily infect preexisting wounds.
•The infection may start in skin that has been
injured due to a scratch or insect bite.
 
•The infection
 often develops on the legs.

23. Presentation
•Ecthyma begins as a vesicle or pustule overlying
an inflamed area of skin that deepens into a
dermal ulceration with overlying crust.
•The crust of ecthyma lesions is gray-yellow and is
thicker and harder than the crust of impetigo.
•A shallow, punched-out ulceration is apparent
when adherent crust is removed.
•The deep dermal ulcer has a raised and indurated
surrounding margin

25. •It is rarely leads to systemic symptoms or
bacteremia.
•Lesions are painful and can have associated
lymphadenopathy.

26. Risk factors
•Immunocompromised states (eg, diabetes,
neutropenia) predispose patients to the
development of ecthyma.
•Spread of skin streptococci is augmented by
crowding and poor hygiene.
•High temperature and humidity

27. Diagnosis
•Gram stain and culture of ecthyma lesions
reveal gram-positive cocci
•Histological finding
•Ecthyma lesions show dermal necrosis and
inflammation.
•A deep and superficial granulomatous perivascular
infiltrate occurs along with endothelial edema.
•A heavy crust covers the surface of the ecthyma ulcer.

28. Management
•Medical treatment for ecthyma depends on the
progression of the lesions
•Hygiene – clean using antiseptic soln
•Topical therapy with mupirocin ointment for
localized lesions
•Oral antibiotics for extensive lesions
•Parenteral antibiotics for widespread ecthyma.
•The leions may require gently debridement of the
crusts.

29. DDX
•Pyoderma Gangrenosum
•Lymphomatoid Papulosis
•Papulonecrotic Tuberculids
•Insect Bites
•Dermatologic Manifestations of Sporotrichosis

30. Complications
•Secondary lymphangitis and cellulitis can
occur.
•poststreptococcal glomerulonephritis in
approximately 1%.

31. Prognosis
•Ecthyma lesions are slow to heal but do
respond to appropriate antibiotics over
several weeks
•Prognosis is favorable.

32. CELLULITIS

33. Cellulitis
•Is an acute spreading infectious process
affecting the skin (epidermis & dermis)
extending into the subcutaneous tissue
•Characterized by Inflammation
•Manifests as erythema, edema, and warmth.
•Systemic manifestation
•Fever, chills, leukocytosis
•Bacteremia up to 30% of cases

34. •It generally due to
•Trauma
•Underlying skin condition

35. Microbiology
•Majority of infections:
Staphylococcus aureus > 80 %
streptococci
•Considerations:
•Methicillin resistant S. aureus (MRSA)
•Vancomycin resistant enterococci (VRE)
•Gram negatives: pseudomonas, E. coli
•Anaerobes: Clostridium, Bacteroides,
peptostreptococcus

36. Risk factors
•Body piercing
•Animal bite
•Immunocompromised
•Diabetes
•IV drug users
•Liposuction

37. Presentation
•Erythema
•Edema
•Warmth
•Tenderness
•Borders are not sharply demarcated
•Regional adenopathy

39. Treatment
If strong suspicion of etiologic agent treat with
specific antimicrobial.
If etiologic agent unknown:
- No underlying risk factors
1st generation ceph (cover Staph and
Strep)
Alternative: if Pen allergic
- Erythromycin or Azithromycin

40. •If MRSA then
1) Clindamycin 300 to 450 mg PO TID
2) Bactrim 1-2 DS tab PO BID
3) Doxycycline 100 mg PO BID
4) Linezolid 600 mg PO BID
•Depends on clinical response but a time
course of 5-10 days is usually appropriate

41. Complications:
•Abscess
•osteomyelitis

42. ERYSIPELAS

43. INTRO
A superficial cellulitis of the skin with prominent
lymphatic involvement
•Superficial cellulitis with extensive lympathic involvement
Occasional spread to deeper structures
Generally due to group A Strep (rarely group C
or G)
•S. pyogenes specifically
•30% of pts. have had a streptococcal respiratory infection

44. Common seen in
- infants
- young kids
- older adults
- immunocompromised
(diabetics, alcoholic, nephrotic
syndrome, venous stasis, paraparesis)
Generally an acute infection with the rash
spread abruptly

45. 70-80% of lesions are on the lower extremity
5-20% are on the face
Portal of entry
•skin ulcers,
•local trauma,
•abrasions,
•primary dermatologic conditions likeTineas

46. Presentation
A painful lesion with a bright red edematous
indurated appearance and an advancing raised
border-sharply demarcated
•Shiny red rash with raised border
•extremely red, warm skin and swollen under the lesion
or sore
•There may be fluid-filled lesions scattered along the
area
Fever
Bacteremia ~ 5%
Leukocytosis very common

48. Management
Penicillin oral vs parenteral
-For 2-3 weeks
Alternatives
- 1st generation ceph.
- Erythromycin or Azithromycin

49. Complication
•Spreading to the joints
•Infection in the blood
•Septic shock
•Recurrent of infection

50. Prognosis
•Is good
•Delay of treatment, however, increases the
chance for bacteremia and the potential for
death from sepsis.
•Immuno compromized patients have more
likely recurrent infection in the same location

51. Summary