Dr. Nathan Muluberhan presented on soft tissue infections. He discussed the anatomy of the skin and its layers. He then summarized various soft tissue infections including impetigo, cellulitis, erysipelas, necrotizing soft tissue infections, and cutaneous abscesses. For each infection, he described the microbiology, risk factors, clinical features, diagnosis, and treatment. He emphasized that soft tissue infections range from superficial to life-threatening and require prompt diagnosis and management.

1. S O F T T I S S U E
I N F E C T I O N S
(seminar)
Dr. Nathan Muluberhan(E M
r e s i d e n t )
Emergency And Critical Care
Medicine
OC T 2017
1

2. OUTLINE OF PRESENTATION
 Anatomy
 Impetigo
 Cellulitis
 Erysipelas
 Necrotizing soft tissue infections
 Cutaneous abscesses
 Pilosebaceous follicular infections
2

3. ANATOMY OF SKIN
 The largest organ in our body,
comprising about 15% of the body
weight & 10% of total circulation
 Layers:
 Epidermis
 Dermis
 Subcutaneous layer (Panniculus)
 Epidermal derivatives (accessory
organs)
 hair follicles
 sebaceous glands
 sweat glands
3

4. Epidermis
Hair shaft
Dermis
Reticular
layer
Papillary
layer
Hypodermis
(superficial fascia)
Dermal papillae
Pore
Subpapillary vascular
plexus
Appendages of skin
Eccrine sweat gland
Arrector pili muscle
Sebaceous (oil) gland
Hair follicle
Hair root
Nervous structures
Sensory nerve fiber
Lamellar (Pacinian)
corpuscle
Hair follicle receptor
(root hair plexus)
Dermal vascular plexus
Adipose tissue
4

5. SKIN AND SOFT TISSUE INFECTIONS
(SSTIS)
 Are inflammatory microbial invasions of the
epidermis, dermis and subcutaneous tissues.
 Described with the classical signs of
inflammation as calor, rubor, tumor, dolor
and fluor (heat, redness, swelling, pain and
discharge)
 Have different classification system
5

6. The practice guidelines of the IDSA for the diagnosis
and management of SSTIs classifies into five
categories:
1. Superficial uncomplicated infection
2. Necrotizing infection
3. Infections associated with bites and animal contact
4. Surgical site infections
5. Infections in the immunocompromised host
CLASSIFICATION CONT…
IDSA: Infectious Diseases Society of Americ
6

7. Based on the severity of local and systemic signs
Class 1: patients have no signs of systemic toxicity and no
uncontrolled co-morbidities;
Class 2: patients are either systemically ill or systemically well but
with co-morbidity.
Class 3: patients may have a significant systemic upset acute
confusion, tachycardia, tachypnoea or hypotension
 Have unstable co-morbidities that interfere with response to
therapy
Class 4: patients have sepsis syndrome or severe life-threatening
infection.
CLASSIFICATION CONT…
7

8. Classification according to the layer affected
 EPITHELIUM: Varicella & Measles
 KERATIN LAYER: Ring worm
 EPIDERMIS: Impetigo
 DERMIS: Erisepelas
 HAIR FOLLICLES: Folliculitis, boils, carbuncles
 SEBUM GLANDS: Acne
 SUBCUTANEOUS FAT: Cellulitis
 FASCIA: Necrotizing fasciitis
CLASSIFICATION CONT…
8

9. 9

10.  Purulent Vs non-purulent
1. PURULENT: Cutaneous abscess, Furuncle,
carbuncles
2. NON-PURULENT: Cellulitis-erysipelas, necrotizing
fasciitis
CLASSIFICATION CONT…10

11. IMPETIGO
 Most prevalent in children aged 2 to 5 years
 It is communicable
 Does not affect mucous membranes
 Impetigo rarely progresses to systemic illness.
 Cause of poststreptococcal glomerulonephritis
 Has two forms nonbullous and bullous
11

12.  NON BULLOUS IMPETIGO Or IMPETIGO CONTAGIOSA:
 is more common
 most cases are due to S. aureus.
 the lesions begin as thin-walled vesicles that
progress to pustules; subsequent rupture results
in the characteristic so-called honey crusted
lesions
 typically found on the face or extremities
 Associated lymphadenopathy is common
IMPETIGO CONT…
12

13.  BULLOUS IMPETIGO
 Caused by S. Aureus, including CA-MRSA
 The bacteria produce an epidermolytic toxin
 Separation of the dermal-epidermal junction; resulting
in bullae
 The lesions in bullous impetigo are fewer and
larger
 After rupture, the bullae leave a thin brown crust
IMPETIGO CONT…
13

14. 14

15.  Treatment of bullous and nonbullous impetigo
should be with either mupirocin or retapamulin
twice daily (bid) for 5 days (strong, high)
 Oral therapy for impetigo should be a 7-day
regimen with an agent active against S. aureus
(strong, high)
 Because S. aureus isolates from impetigo are usually
methicillin susceptible, dicloxacillin or cephalexin
TREATMENT
15

16.  When MRSA is suspected or confirmed,
doxycycline, clindamycin, or sulfamethoxazole-
trimethoprim (SMX-TMP) is recommended
(strong, moderate)
 Systemic antimicrobials should be used for
infections during outbreaks of
poststreptococcalglomerulonephritis
 Eliminate nephritogenic strains of S. pyogenes from
the community (strong, moderate).
TREATMENT CONT…
16

17. CELLULITIS
 Accounts for approximately 1.3% of all ED
visits
 Observed more frequently among middle-aged
and elderly patients.
 Male predominance (61%)
 Mean age of 46 years
 Approximately 10% of patients diagnosed with
cellulitis are hospitalized
17

18. MICROBIOLOGY
 80% of cellulitis cases are caused by gram-
positive bacteria.
 Community-acquired MRSA is now the most
common cause of skin and soft tissue infections
presenting to the ED
 Gram-negative aerobic bacilli are the third most
common etiology
18

19.  General Risk Factors for Cellulitis and Erysipelas
 Lymphedema
 Skin breakdown/site of entry
 Venous insufficiency
 Leg edema
 Obesity
 Neutropenia
 Immunocompromise
 Hypogammaglobulinemia
 Chronic renal disease
 Cirrhosis
CELLULITIS CONT…
19

20. 20

21. PATHOPHYSIOLOGY
 Most symptoms are 2nd to complex set of
immune and inflammatory reactions triggered
by cells within the skin itself.
 Infiltration of cells, such as Langerhans cells
and keratinocytes, releases the cytokines
(interleukin-1 and TNF) that enhance skin
infiltration by lymphocytes and macrophages
21

22. CLINICAL FEATURES
 Symptoms develop gradually over a few days
 The affected skin is tender, warm,
erythematous, and swollen, and typically does
not exhibit a sharp demarcation from
uninvolved skin.
 Edema can occur around hair follicles that
leads to dimpling of the skin
 an orange peel appearance to as “peau d’orange”
22

23. 23

24.  In cases of purulent cellulitis, exudate drains from
the wound.
 Systemic signs of fever, leukocytosis, and
bacteremia are more typical in the
immunosuppressed.
 Recurrent episodes of cellulitis can lead to
impairment of lymphatic drainage, permanent
swelling, dermal fibrosis, and epidermal
thickening.
 These chronic changes are known as elephantiasis
nostra
24
CLINICAL FEATURES CONT…

25. 25

26. DIAGNOSIS
 The diagnosis of cellulitis is clinical
 In cases of mild infection, blood cultures, needle
aspiration, punch biopsy, leukocyte count, or other
lab data are of little benefit and are not
recommended.
 Needle aspiration of the leading edge of an area
of cellulitis produces organisms in 15.7% of
cultures
 Punch biopsy reveals an organism only 18% to
26% of the time.
26

27.  Wound culture is recommend when patient are on antibiotics
for purulent cellulitis.
 Blood cultures are positive in only 5% of cases.
 Cultures of pus, bullae, or blood are recommended for both
purulent and non purulent cellulitis:
 With systemic toxicity
 Extensive skin involvement
 Underlying comorbidities
 Immunodeficiency
 Failed initial therapy, or recurrent episodes, or in circumstances
such as animal bites
DIAGNOSIS CONT…
27

28.  Routine radiographic evaluation is unnecessary
 Unless osteomyelitis or necrotizing soft tissue infections are
suspected
 Bedside US is useful to exclude occult abscess
 Doppler may help to distinguish lower extremity
DVT from cellulitis
DIAGNOSIS CONT…
28

29. TREATMENT
 General Treatment
 Elevation of the affected area
 Incision and drainage of any abscess found
 Antibiotics
 Treatment of underlying conditions.
 Treat skin dryness with topical agents .
29

30. 30

31. 31

32.  Systemic corticosteroids (eg, prednisone 40 mg
daily for 7 days) could be considered in
nondiabetic adult patients with cellulitis (weak,
moderate).
 Administration of prophylactic antibiotics, such as
oral
penicillin or erythromycin bid for 4–52 weeks, or
IM
benzathine penicillin every 2–4 weeks.
 should be considered in patients who have 3–4
TREATMENT CONT…
32

33. DISPOSITION AND FOLLOW-UP
 Admit patients with:
 Evidence of systemic toxicity
 Underlying comorbidities such as DM, alcoholism, or
immunosuppression
 Patients without systemic toxicity can be
discharged with follow-up
 Mark the patient’s skin along perimeter of infection so
healing can be determined at follow-up.
33

34. ERYSIPELAS
 Involves the upper dermis and superficial
lymphatics
 usually caused by β-hemolytic streptococci
 Bullous erysipelas is a more severe form
 represent synergy with B-hemolytic streptococci
and methicillin-resistant staphylococcal aureus.
34

35. CLINICAL FEATURES
 Usually abrupt onset prodromal phase.
 With fever, chills, malaise, and nausea
 Over the next 1 to 2 days, a small area of
erythema with a burning sensation develops
 As infection progresses, the affected skin
becomes indurated with a raised border that is
distinctly demarcated from the surrounding
normal skin
35

36. 36

37. NECROTIZING SOFT TISSUE
INFECTIONS
 A spectrum of illnesses characterized by
fulminant, extensive soft tissue necrosis,
systemic toxicity
 Early in their course, these infections can
appear deceptively benign
37

38. RISK FACTORS
 Advanced age
 Diabetes mellitus
 Alcoholism
 Peripheral vascular
disease
 Heart disease
 Renal failure
 HIV
 Cancer
 NSAID
 Decubitus ulcers
 Chronic skin infections
 IV drug abuse
 Immune system
impairment
38

39. MICROBIOLOGY
 Type I (polymicrobial) infections
 55% to 75% of all necrotizing soft tissue infections
 combination of gram-positive cocci, gram-negative rods, and
anaerobes.
 Type II (monomicrobial) infections
 most commonly caused by group A Streptococcus.
 20% to 30%
 often has a history of trauma or has had a recent operative
procedure
 CA- MRSA is a cause particularly in IV drug abusers, athletes,
and institutionalized patients.
39

40.  Type III infection
 Caused by Vibrio vulnificus.
 More common in Asia
 Type IV infection
 Associated with fungal infections
 Primarily in immunocompromised patients
MICROBIOLOGY CONT…
40

41.  Bacteremia is reported in 25% to 30% of cases
 a strong predictor of mortality
 Other patient factors that increase mortality are
 age <1 year old or >60 years old
 comorbid conditions, especially cancer, CKD and CHF
 IV drug use
 certain characteristics of the clinical course
 positive blood culture,
 trunk or perineal involvement,
 infection related to peripheral vascular disease
 delayed time to diagnosis or treatment
41

42. PATHOPHYSIOLOGY
 Necrotizing process typically begins with
 Direct invasion of subcutaneous tissue from
external trauma
 Direct spread from a perforated viscus
 Bacteria proliferate, invade subcutaneous
tissue and deep fascia, and release exotoxins
that lead to tissue ischemia, liquefaction
necrosis, and systemic toxicity
42

43.  Infection can spread as fast as 1 inch/h
(2.5cm/h)
 The ischemic tissue environment promotes
bacterial growth, propagating the process and
resulting in rapid spread of the infection.
 impedes immune system destruction of bacteria
and prevents adequate delivery of antibiotics
PATHOPHYSIOLOGY CONT…
43

44.  Skin involvement is secondary to vasculitis and
thrombosis of perforating blood vessels.
 Large numbers of capillary beds thrombosis must
occur before skin findings develop
 Early infection has little overlying skin change to
indicate the extent of infection.
 As the disease progresses, widespread gangrene
of the skin, subcutaneous fat, fascia, and even
skeletal muscle occurs
PATHOPHYSIOLOGY CONT…
44

45. CLINICAL FEATURES
 Classic symptoms of necrotizing soft tissue
infections are severe pain, anxiety, and
diaphoresis.
 Pain is often out of proportion physical
examination findings
 Tenderness beyond the area of erythema
 The single most important feature to make the
diagnosis early
45

46.  The painful area may demonstrate edema, and
crepitus
 The lack of crepitus does not rule out the
diagnosis.
 Later, the skin can develop a bronze or
brownish discoloration with a malodorous
serosanguineous discharge, and bullae may
be present
CLINICAL FEATURES CONT…
46

47.  Systemic manifestations include
 low-grade fever with tachycardia
 Cardiovascular collapse (particularly from V.
vulnificus),
 Confused, irritable, or have a rapid deterioration
of mental status due to
 Release of bacterial toxins
 Release of cytokines
CLINICAL FEATURES CONT…
47

48. DIAGNOSIS
 The diagnosis is based on clinical assessment
in combination with laboratory tests and
imaging.
48

49.  One or more “hard” signs of necrotizing
fasciitis
 crepitus
 skin necrosis
 bullae
 hypotension
 gas on x-ray
Present in less
than half of
patients
DIAGNOSIS CONT…
49

50. 50

51. 51

52. THE 'FINGER TEST
 A positive test
 The absence of normal blood flow
 Dirty 'dishwater' colored fluid
 Discoloration of the fat would
 Friable tissue to minimal finger pressure
52

53. TREATMENT
 Aggressive fluid resuscitation immediately
 Transfusion of pRBC may be needed to correct
anemia from hemolysis.
 Avoid vasoconstrictors,
 if at all possible, because vasoconstrictors will
decrease perfusion to already ischemic tissue.
 Early surgical consultation is indicated for all
suspected cases of necrotizing fasciitis.
53

54. TREATMENT CONT…
 Surgery is the gold standard for diagnosis and
treatment
 Surgical intervention may include
 fasciotomy, debridement, and/or amputation
 Mortality is high if debridement is delayed >24
hours
54

55. CUTANEOUS ABSCESSES
 Skin abscesses typically begin as a local
superficial cellulitis.
 MRSA causes the majority of skin abscesses
presenting to the ED in the US
 Loculation and subsequent walling off of
leukocytes and cellular debris response to the
infection lead to abscess formation.
55

56. CLINICAL FEATURES
 Fluctuant, tender, erythematous nodules,
often with surrounding erythema.
 Spontaneous drainage of purulent material
may occur, and local lymphadenopathy may
be present.
 Signs of systemic toxicity, fever, or chills are
rare in the case of simple abscesses.
56

57. DIAGNOSIS
 Diagnosis is clinical; however, physical exam is
unreliable for non-superficial abscesses
 Bedside US is an invaluable tool
 For distinguishing deep abscess from cellulitis
 Identifying a foreign body within an abscess
 Determining the adequacy of drainage
 Radiography is not needed routinely
 unless a radiopaque foreign body or underlying
osteomyelitis is suspected.
57

58. 58

59. TREATMENT
 It is best to drain extremely large abscesses or
those in deep areas in the OR
 Abscesses of the palms, soles, or nasolabial
folds usually require a specialist.
59

60.  Antibiotics are generally unnecessary after I & D
of uncomplicated abscesses.
 Guidelines recommend antibiotics for patients
 With multiple lesions
 Extensive surrounding cellulitis
 Immunosuppression
 Signs of systemic infection
I & D: incision and
TREATMENT CONT…
60

61. DISPOSITION AND FOLLOW-UP
 Most patients with skin abscess are treated
outpatient.
 remind patients to keep the wound covered
 practice frequent hand washing
 Individuals should not share items such as towels,
clothing,
soap…
 Those with systemic toxicity or severe infection
may require parenteral treatment and hospital
admission.
61

62. PILOSEBACEOUS FOLLICULAR
INFECTIONS
 Folliculitis, furuncles, and carbuncles are
purulent infections originating in the hair
follicle.
 Acne and hidradenitis suppurativa (acne
inversa) result from the obstruction of
sebaceous glands
62

63.  A superficial inflammation of the hair follicle that is
limited to the epidermis.
 Usually due to infection of s. Aureus
 It can affect any hair-bearing area of the skin.
 The diagnosis is made clinically
 its characteristic appearance of a small (2–5 mm),
raised, erythematous, painful, tender lesion that is
typically pruritic.
FOLLICULITIS
63

64.  Hot tub folliculitis: caused by Pseudomonas
aeruginosa that develops within 48 hours of
bathing in a contaminated hot tub or swimming pool
or from use of contaminated sponges.
 Eosinophilic folliculitis: is a noninfectious
recurrent disorder.
 It is more likely to occur in immunocompromised
patients and is considered an AIDS-defining
FOLLICULITIS CONT…
64

65. TREATMENT
 For simple cases of uncomplicated
 stopping exposure or removing the offending agent
 twice-daily cleansing with mild hand soap often suffices
 if desired, warm compresses may be applied several times
daily, and a topical antibiotic such as bacitracin or polymyxin
B can also be used.
 Shaving should be avoided in the involved areas.
 More extensive cases, oral antibiotics with activity against
Streptococcus and Staphylococcus, (such as cephalexin,
dicloxacillin, or azithromycin, are recommended)
65

66. FURUNCLES
 an infection of the hair follicle in which suppuration
extends through the dermis into the subcutaneous
tissue
 are painful and erythematous and often drain
spontaneously.
 The most common cause is S.aureus, both
methicillin-sensitive and CA-MRSA.
66

67. CARBUNCLES
 Comprises multiple furuncles with loculations
and connecting sinuses, often with multiple
sites of drainage.
 Are more likely to occur on the back of the
neck and are more prevalent in diabetics.
67

68. 68

69. TREATMENT
 Furuncles and carbuncles are treated in the
same manner as skin abscesses.
 There is insufficient evidence to recommend
for or against antibiotics
 Rosen’s suggest coverage for streptococci and
MRSA when disease is severe.
69

70. REFERENCEs
70

71. 71