NECTOTIZING SOFT TISSUE INFECTIONS

Diagnosis and Treatment

Hugh M. Foy, M.D.

Attending Surgeon
Harborview Medical Center
University of Washington

Necrotizing Soft Tissue Infections

( NSTI )

OBJECTIVES
Anatomy and physiology
Common Pathogens strategy
Be able to recognize:
Patients at increased risk
Early Symptoms and Signs

Review Principles of Treatment

Necrotizing Soft Tissue Infection

NSTI

Terminology and Nomenclature

History
Pathogenesis
Clinical Presentation
Diagnosis
Treatment

Necrotizing Soft Tissue Infections

NOMENCLATURE
Clostridial
Non-Clostridial

Pure Strep (GAS)

Mixed Infections

Strep and Friends (Enterobacteracie)

Fourniers
Melanies Staph-Strep

Nomenclature
Chronic gangrene
Necrotizing fasciitis

Gas gangrene
Streptococcal gangrene
Bacterial synergistic gangrene
Anaerobic cutaneous gangrene

Fournier's gangrene

Clostridial cellulitis

Non-clostridial
anaerobic cellulitis
Meleney's synergistic
gangrene
Gangrenous erysipelas

Progressive synergistic
gangrene

STOP

Postoperative synergistic
gangrene

Synergistic necrotizing cellulitis

Necrotizing Soft Tissue Infections

HISTORY

1871- Jones
US Civil War Hospital gangrene
1883 - Fournier
Involvement of the male genitalia
1924 - Meleney
Hemolytic streptococcal gangrene
1952 - Wilson
Necrotizing fasciitis

RISING INCIDENCE OF
NSTI
Selection pressure
of antibiotics
Diabetes
Obesity
Changing patterns
of IVDU

IV Drug Use (IVDU) - Related

NSTI
Bosshardt, Arch Surg, 1996

16
14
12
10
IVDU
Other

8
6
4
2
0

1990

1991

1992

1993

1994

1995

Soft Tissue Wounds

Lacerations
Puncture Wounds
Avulsions
Abrasions

Puncture Wounds
Deeper than wide

Full thickness through

skin and into
subcutaneous fat
Fat has the poorest
blood supply
Anaerobic bacteria
thrive in areas of low
O2

QuickTime and a
YUV420 codec decompresso
are needed to see this pictur

Clostridia
Micro aerophilic and
anerobic Strep

Avulsions
Tissue is torn away

Trap door laceration

Semi-sharp object snags

and tears the skin

Degloving Injury

Sheering force rips fat

and skin off of the
muscle fascia
Common after being run
over by tire
Classically: wringer
injuries
Bruising, loose skin,
dead fat

Anatomical Considerations
Skin receives its
blood supply from
Myofascial
perforators

Out from the muscle,

through the fascia,
Through the sub
cutaneous fat
Arborizes in the
subdermis and dermis

Subcutaneous Fat and

Fascia
Poorest blood supply

Fat outgrows its blood supply

Surgical Infections
Definition:

Result when host defenses overcome:

those infections which require operative drainage or

debridement

Examples:

Abscesses
Necrotizing Fasciitis
Clostridial Myonecrosis
Necrotic Debris

Bacteriology 101
Reproductive Strategies
K dependent organisms
Few offspring, lots of
nurturing
Primates, whales,
elephants

R dependent organisms
Make lots of offspring,
little nurturing

Fish, Bugs, bacteria

Bacteriology 101 (cont.)

Bacteria have needs too:

Transportation
Shelter, protection
Food, nutrition
Utilize unique habitats to
avoid competition

but have a limited repertoire of survival

strategies

Survival Strategies
Transportation

Make slime, like we make concrete

Protect themselves

Special coatings encapsulated

organisms
H. flu, mennigeococci,
pneumococci
WBCs cant stick to them
Immunologic disguise

Kill antibiotics-penicillinase,

Utilize their niche

Make enzymes and toxins to take

advantage of specific host
environment

Bacterial diversification
utilize various niches to avoid competition

Metabolic Machinery
Aerobes

Need O2 to make energy (ATP)

Anerobes

Thrive in O2 depleted environment

Love dead tissue- help break it down
Helpful if in the casket or the garden
lethal in your wound

Enzymes and toxins

the key to understanding bacterial pathophysiology

Dissolve Protein

Hyaluronidase, protease, lecithinase,

collagenase

Alter coagulation

Cause coagulation- Staph

Coagulase- creates a zone of avascularity (abscess)

Dissolve clots- Streptokinase

Cellulitis is often heralded by petechiae

Early Strep
hemolysis/petechiae

Infection
Usually results when
bacteria overcome
host defenses
Adequate blood supply
Primary Local defense

Secondary Defense
WBCs, Macrophages

Race against the

clock:

Rate of bacterial proliferation

vs neovascularization

Neovascularization
Fat has a poor
blood supply
After 4 to 5 days,

Capillaries begin to
grow and form
granulation tissue
After the fat is
covered, the wound
can be closed, as
the local defense is
more capable

Surgical Infections
Abscesses

Staph and friends

Cellulitis

Strep, Coliforms, Clostridia

Toxic Shock Syndromes- Staph and Strep

Hospital Gangrene
Synergistic Staph-Strep Gangrene
Necrotizing Fasciitis
Pure Strepcoccal Gangrene
Necrotizing Soft Tissue Infections
Clostridial Myonecrosis

Streptococcal Infection

Cellulitis
Lymphangitis
Necrotizing Fasciitis

Abscess

Staph-Strep Synergistic Gangrene

Melanies Ulcer

Persistent
Cellulitis
Full thickness
Punched out
ulcers
Microaerophilic
Strep and Staph

Diffuse fluctuance,
undermined edges

Require Unroofing, drainage

NSTI

Group A Beta-Hemolytic Strep

GAS

History

Emergence of more virulent strains

Flesh eating bacteria

1986 Superinfection of Chicken Pox pts

Thought to be result of viral plasmid
insertion into Strep DNA resulting in more
potent toxin

NSTI:
Presentation:

Diagnosis

early: severe pain, out of proportion to skin

findings
later: echymosis, peaudorang, hemorrhagic
blisters
Marked edema
Fever
Leukocytosis

Pure Streptococcal
Gangrene
Less common than mixed infections
May seed hematogenously:
strep throat or other infection
to an area of poor blood supply
to an area of previous minor trauma
Late recognition in dark-skinned
patients

NSTI Diagnosis

Presenting Symptoms and

Signs

Clinical Features:
Skin changes
Thin, purulent
drainage
Thrombosis of
small vessels
Easy finger
dissection along
fascial planes

Dermal edema, thrombosis,

hemorrhagic blisters

NSTI

Diagnosis

Usually a clinical diagnosis

Pain out of proportion
Marked edema
Skin Changes

Fever
Leukocytosis

NSTI

Diagnosis
Clinical features
Lab
Xray
Wound Exploration

NSTI Diagnosis

Radiographic Studies
Plain Films
? Gas?

CT Scan

Helpful to note extent

MRI

Helps the non-surgeon

Should not delay operative debridement!

NSTI: Diagnosis

Finger Test

LRINEC for diagnosis of NSTI

Wong, Crit Care Med, 2004
Variable

Score

C-reactive protein
<150

>150
WBC

<15

15-25

Variable

Score

Sodium
>135

<135
Creatinine

<141

>141

>13.5

Glucose

11-13.5

<10

<11

>10

>25
HgB

Mixed NSTI
Usually a micro-aerophilic strep with
other enteric organisms
Fourniers Gangrene
Foul smelling drainage
Elderly, obese, diabetics

Fourniers Gangrene,

skin changes often an understatement

Fourniers-

after debridement

Fourniers Gangrene

NSTI:

Treatment

Early Recognition
Resuscitation
Antibiotics
Surgical Debridement
Reconstruction

A team approach: tough nurses, intensivists, surgeons,

reconstructive
surgeons

NSTI:

TREATMENT

Empiric treatment should cover:

Strep, Clostridia and Gram Negatives

Penicillin 6 million units q4h
Strep, clostridium

Clindamycin 1200 mg q6h

Anaerobic coverage (clostridium)

Protein synthesis inhibitor reduces toxin production

Gentamicin (or ciprofloxacin)

Gram negative

Consider vancomycin if endemic MRSA

Timely, appropriate antibiotic treatment correlates with
lower morbidity and mortality

NSTI Treatment:

Antibiotic Alternatives
Metronidazole
Fluoroquinolones
Aztreonam

NSTI Treatment

SURGICAL DEBRIDEMENT
PROMPT

ASAP after admission

AGGRESSIVE

Debride back to healthy tissue

REPEAT DAILY UNTIL CLEAN

Scheduled take back the next day

Be bloody,
bold and resolute

Shakespea

NSTI Treatment

Adjunctive Therapy
Activated Protein C
IV Ig
Plasmapheresis
Hyperbaric Oxygen

Ready for Skin Grafting

Clostrial Infection

Lives in the soil and in the colon

Obligate Anaerobe
Produces potent toxins
Broad Clinical Spectrum of disease
Fatal if not promptly recognized and
aggressively treated

Clostridial Infection
Gram Positive, Spore-forming Rod
Route of entry:
Puncture wound
Colon perforation
Fecal contamination

Clostridial Infections

Cellulitis- C. novii
Tetanus- C. tentani
Botulism- C. botulinum
Myonecrosis- C. perfringens
Hematogenous- C. septicum
Pseudomembranous Entercolitis
C. dificil

C dif
Enterocolitis

Clostridial Myonecrosis

CLINICAL PRESENTATION
Severe Pain

out of proportion

Faint, pale erythema

Thin, dish-water drainage
Foul, musty smelling
Marked edema and induration
Hemorrhagic Blisters
Gram Stain- Gm + Rods, minimal WBCs
? Hyponatremia
? Leaping WBC

Clostridial Infection

PATHOPHYSIOLOGY

Thrives in anaerobic environment

Produces 14 identified toxins
Produce H2, CO2 and N2 gas
Induce potent leukotriene production

Gas Gangrene

Clostridial Pathophysiology

Toxins
Alpha Toxin

Exotoxin
Phospholipase

hemolysis, cytotoxic to PMNs

Inhibits chemotaxis,
Degrades sphingomyelin
Microvascular thrombosis
Lyses phagocytes- releases organisms and stim ILs

Theta Toxin- cytolysin

Mu Toxin- hylauronidase

Clostridial Myonecrosis
Impalement injury

Clostridial Infection

TREATMENT

Critically ill patients: ABCs!

Avoid pressors
Rx Coagulopathy
Antibiotics- High dose Penicillin
Prompt, aggressive surgical debridement
Adjunctive Treatment?

Hyperbaric Oxygen
Activated Protein C
Plasmapheresis
IV IG

IVDU and NSTI

Black tar heroin

Mexico, West Coast of US

Dark, gummy form of heroin, cheaper
than white powder
Frequently mixed with diluents
Dextrose, burned corn starch, instant
coffee dirt
Bacterial spores introduced

Epidemics due to batches of bad

heroin

IVDU and NSTI

Polymicrobial in 78%

B-hemolytic strep & S. aureus (49%)

Monomicrobial:

S. aureus 30%, GrpA Strep 22%, Clostridium 30%,

anaerobes 11%

Anaerobes in 67%

Most often Clostridium sordelli, perfringens or novyi

Peptostreptococci, bacteroides

IVDU - related NSTI

CDC, MMWR, 2000

88 cases of clostridium novyi in England,

Scotland and Ireland, Apr-June 2000
Sustained hypotension, median WBC of 63
Clostridium novyi, perfringens
Mortality 45%

IVDU and NSTI

IVDU and NSTI

HMC review
May 1996- July 2001
166 patients

30% IVDA
24% Diabetic
20% Surgical/traumatic wound
infections

Anaya, et al Arch Surg 2005; 140:151-157

Etiology
IVDU
30%

Site of Infection

39% Lower ext

16% Upper ext
13% Abdominal wall
12% perineum
9% Buttock

Outcome
Mortality 17.4%
Predictors of Mortality

Age >65 OR 4.6 CI: 1.1-19

Admission Cr>2.0 OR 3.6 CI: 1.2-11
Admission wbc >40 OR 3.5 CI: 0.9-14
IVDA OR 3.3 CI: 1.1-10
Clostridial infection correlated with leukocytosis and
carried a 50% mortality

45
40
35
30
25
20
15
10
5
0
<5

5 to20

20 to 30

30 to 40

>40

Clostridial Infection

Clinical Dilemmas
Radical Amputation
Delayed Washout of Toxins
Adjunctive Therapy

Nursing Considerations
Wound care training
Logistics
Facilities
Staffing
Materials
Staff Retention

Necrotizing Soft Tissue

Infections
Increasing incidence
Patients at risk:

Diabetics, obese, IDU, puncture wounds

Symptoms:

Severe pain, sepsis, rapid onset

Signs:

Dermal edema, echymoses, necrosis

High index of suspicion,

early recognition and consultation

Summary:

Treatment of NSTIs

Resuscitation, Antibiotics
Surgical Debridement
Prompt
Aggressive
Repeated

Reconstructive Surgery

Clostridial Infection

Case report
63 y.o. woman

3 weeks of abdominal pain,

recent AODM

Incisional hernia

25 yrs s/p TAH for Uterine CA

Gangrenous, colon and small bowel

Lap, resection and debridement of
abdominal wall
Plasmaphoresis

Case 1 (cont)
Admit labs

Na 128, Gluc 339, WBC 16.7

CT of the abdomen:
Extraluminal gas
Small bowel obstruction

Case 1 (cont)
Operative treatment
Expl lap

Small bowel resection

Debridement of abdominal wall
Temporary Abdominal Closure

Post Op
WBC rose to 26k
Plasmapheresis

Post op day 8

Post Op Day 8

SIS fascial replacement and

VAC

Post Op Day 20

Guess that Infection

Melaneys Synergistic
Staph-Strep Gangrene