Necrotizing_Fasciitis_Case
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Necrotizing Fasciitis
VH
• CC: ER on 3/18/2006 with Abdominal Pain
• 43 y/o M Hx Sarcoid (2/2003) off steroids since 1/2004
recently for elective repair of left inguinal hernia on
3/8/2006 after 6 months of increasing symptoms, bulging,
and pain last month.
• Presented to ER with severe abdominal pain though did well
initially postop, NL Bowel function, Flatus, BM POD #2,
decreased pain, ambulation.
• POD #6 increased pain left abd, flank, and scrotum Rad to
anterior Abd worse standing. Anorexia. Constipation.
• POD #8 + N/V Bilious. POD #9 Insomnia, Night sweats &
Chills, tactile fever. Less pain at incision, severe upper
abdomen and chest. POD #10 wife insisted on ER.
VH
• PMedHx:
Sarcoid (off steroids)
PUD (H. pylori 1997)
Chronic back pain (MRI:
mild disc protrusion C4-6)
OA
• PSurgHx:
Left ACL 3/2003
Direct LIH Repair
3/8/2006 (plug/patch.
Kefzol)
• FHx: Mother DM II
• SocHx: Negative x 3
Building Maintenance
Sexually inactive
currently (in therapy)
• Allergy: Shellfish
• Meds: Pulmacort,
Celebrex, Alleve
(Prednisone 40 QD wean
off since 1/2004)
VH 3/18/06
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Phys Exam:
A & O X 3. Pain 10/10.
Tmax 40.3, BP: 105/79, P: 130-159, RR 18, 100% RA
HEENT: Perla, EOMi.
PULM: CTA B/L
CVA: S1S2 Tachy.
ABD: Distended, Diffuse (LUQ>LLQ), severe tender
with min. palp and movement. Pos. Guard & Rebound.
Incision C/D/I (epithelialized with NO erythema, skin
changes, nor fluctuance). No Hernias. Sm. Sub Q
emphysema LUQ under rib cage.
Rectal: Heme neg. NL tone & brown stool.
VH
LABS
• WBC 19.9 (60% N),
HCT 42.9, Plt 325
• Na 132, K 4.0, Cl 93, CO2
20, BUN 22, Cr 1.6,
Glucose 133
• PTT 36, INR 1.3
• ABG: 7.41/29/82/18/97.6
Lactate: 2.0
Port CXR: b/l hilar LAD,
No Free air, no change
VH: Cat Scan
VH Cat Scan
VH Cat Scan
VH: Pink Slip
• CT: Large air, fluid, debris collection
(26x14x3.4 cm) left lateral anterior Abd
Wall from Left inguinal region to left ext
iliacs up to left level of the ribs. Dilated SB
c/w ileus
• Received in ED: Hi dose PCN, Flagyl
500mg, Rocefin 1Gm. Analgesia. IVF’s
• Consent obtained, Category 1 Pink Slip
• In Holding: Clinda 300 mg, Ampicillin 2 G,
• ID consult started Zosyn.
• Diag Lap: Small
segment of sig colon
adherent to left inguinal
hernia repair area with
only local inflam. No
pus nor frank SN’s of
infection intra-abdom.
• Prev hernia incis open
foul smelling pus.
Necrotic fascia sent
specimen w/Cx. Incis
extended 25 cm lat up to
rib cage. Mesh
removed
• Necrotic subcut and
fascia debride to viable
tissue & pulse lavage
VH
To SICU post op.
• POD #1: T 39.4 > 36.5
Tachy 101. 110/60. Good
u/o. Extub. WBC 11.4
Dressing change min.
fibrinous exudate, viable
tissue. QD dress change.
GS: Gram neg bacilli.
• POD #4: Afeb. WBC 14.3.
Some fibrin material,
Washout OR.
Cx: Eikenella (likely with
strep per ID)
• POD #6: Afeb doing well.
Vac dressing. WBC 12
• POD #10:
VH
Necrotizing Fasciitis: Without
Boundary
• Characterized by fulminant destruction of tissue,
systemic signs of toxicity, and a high rate of
mortality. Extensive tissue destruction,
thrombosis of blood vessels, abundant bacteria
spread along fascial planes, and an unimpressive
infiltration of acute inflammatory cells.
• “Anatomically…marked by a layer of necrotic
tissue, which is not walled off by a surrounding
inflammatory reaction and thus does not present a
clear boundary.”
-Sabiston
A rose by any other name…
• Necrotizing cellulitis
• Gas Gangrene (clostridial
myonecrosis)
• Necrotizing fasciitis Type I
• Necrotizing fasciitis Type II
Necrotizing Cellulitis
• Clostridial Cellulitis
Usually C. perfringens Preceded by local trauma
or surgery. Gas found within skin, but fascia and
muscle are spared. Crepitus. Less toxic.
• Non-clostridial anaerobic cellulitis
Mixed anaerobic and aerobic organisms produce
gas. Usually in Diabetics. Foul Odor.
• Must be distinguished from myonecrosis and Nec.
Fasc. through surgical exploration (ASAP).
Clostridial Myonecrosis
• Spontaneous Non-traumatic Gangrene:
C. Septicum. GI lesion. (Diverticulitis Colon CA)
67-100% mortality usually in 24 hrs.
• Traumatic Gas Gangrene: usually deep
penetrating trauma, compromise to blood supply,
creating anaerobic environment Req.
• 50% Civil War GSW. Est 30-80% open wounds Cx
Clostridm. sp -Maclennan 1962
• 80% caused by C. perfringens.
• Assoc. with bowel/biliary surgery, retained
placenta/products of conception, aseptic abortion,
intramuscular epinephrine injection, skin popping
• Recurrence after 10-20 years has been reported
Traumatic Gas Gangrene
• Tissue damage introduces vegetative or spore forms
and provides optimum low ox/reduction potential &
acid pH.
• Necrosis progresses 24 - 36 hrs. PMNs become
sequestered & adhere to capillary endothelium never
making it to necrotic jnctn
• Alpha Toxin: Lethal, Hemolytic, Phospholipase C
activity (PLT, leuk, fibrin aggregates decrease skeletal
muscle flow & suppress myocardium)
• Theta Toxin: Hemolytic, vasodil “Warm shock”
Clinical
• Sudden severe pain. Mean incubation 24
hours (range 6 hours to several days)
• Skin initially appear pale, quickly changes
bronze/purple red, tense & tender. Clear, red,
blue, or purple bullae.
• Systemic toxicity low fever, tachycardia,
diaphoresis > shock.
• Crepitus > OR. CT & MRI deep tiss & uterus
• Gram stain: variable rods from specimen (G+
from media)
Treatment: No Controlled Trial
• Debride down to viable tissue that bleeds and
muscle that contracts with bovie
• Clindamycin provides greater viability than
PCN. Clinda + PCN greater than either alone
in animal studies (2-5% Clostridial sp resist
to Clinda) -Stevens 1987
• Gas gangrene of extremity better prognosis
than abdomen. Avoid epinephrine, long
tourniquet use. Leave wound open. Pressor?
• Hyperbaric Oxygen: No Data
Type I Necrotizing Fasciitis
• Usually Diabetics, PVD, Immunocompromised
or postoperative with portal of entry
• Mixed infection caused by anerobes and aerobes.
Avg > 4 isolates. Synergists. Most common Staph
aureus, strep, enterococci, E. Coli, Bacteroides,
Peptostreptococcus, Prevotella
• DM: often of feet with rapid extension up leg.
Consider with cellulitis and systemic signs.
• Fournier’s gangrene: Perineal area. From gi or
urethral organisms. Abrupt spread to anterior abd
wall, gluteal muscles, scrotum, and penis.
Type I cont…
• Ludwigs Angina: Cervical
necrotizing fascitis from mouth flora.
• OK to CT & MRI first. Airway.
• G + aerobic cocci and anaerobes of oropharynx
generally susceptible to PCN (though GAS can
migrate from tonsils)
• In contrast, Type I Nec. Fasc. below the
diaphragm (Bacteriodes & enterobacteriacea)
requires ampicillin plus clindamycin and a
fluoroquinalone.
Type II Necrotizing Fasciitis
• Mono-microbial caused by group A strep (Strep.
pyogenes) And Less Common MRSA
• Any Age with or without PMHX
• Associated with Hx blunt trauma, chickenpox,
NSAIDs, IVDU, penetrating injury, burns, and
surgery.
• Can occur without portal through likely
hematogenous spread from pharynx
• GAS highly contagious microbe causes epidemics of
pharyngitis, scarlet fever, rheumatic fever, and
wound infections. Close contacts have a higher risk
than general population (though still low)
Type II: Group A Strep Virulence
• M proteins: cell membrane protein. Type 1 and 3
most common and can produce pyrogenic
exotoxins or superantigens which can, bind
MHC class II portion of antigen presenting cells
(macrophages and T-cells) without classic
processing by macrophage.
• Rapid proliferation of T-Cell subsets producing
large amounts of TNF alpha, IL1, IL2, TNF beta
• Shock, organ failure, tissue destruction leading to
Strep Toxic Shock Syndrome
Cohen & Powderly. Infectious Diseases. 2004
Type II: Group A Strep
• Rapid Progression, Extensive tissue destruction,
First sign usually severe pain before any cutaneous
findings. 24-48 hrs erythema darkens to reddish
purple, frequently with blister and bullae. With
bullous stage already extensive fasciitis.
• Sometimes without cutaneous findings. But
Systemic Signs first if deep.
• Elevated CK, Cr, and WBC with left shift.
• CT show soft tissue swelling. Often NO GAS
NOR Apparent Abscess.
• 10 % have crepitus. Shock. ARDS. Renal failure.
Cohen & Powderly. Infectious Diseases. 2004
Surgically Debride, ABX, ICU
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Profound hypotension, diffuse capillary leak,
massive ivf’s may be needed despite anasarca, as
much as 10-20 liters per day, mech vent, HD,
Pressors?
Clindamycin better than PCN because:
Clinda is not affected by inoculumn size/stage
growth (PCN binds during stationary phase of
growth)
Clinda Suppresses Toxin Production, &
Inhibits M-protein & cell wall synthesis, & has
Long post antibiotic effect
-Stevens et al. Int J Antimicrob Agents
Cohen & Powderly. Infectious Diseases. 2004
Type II: IVIG
• Intravenous Gamma Globulin to neutralize
circulating strep toxins.
• In 21 GSA patients given IVIG when
hypotensive with 28 day mortality of 33%
compared to Hx rate of 66%. (Though these
patients were more likely to have early
surgical intervention and clindamycin)
-Kaul et al. Clin of Infect Dz. 1999
Mortality Rates
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Type I: 21%
Type II: 30-34%
Cervical: 22-40%
Fournier’s 22-40%
Cohen & Powderly. Infectious Diseases. 2004
General Rec’s
• Resect necrotic tissues, antibiotics, hemodynamic
support
• Emperic abx should cover aerobic and anaerobic.
Ampicillin or Unasyn plus Clinda or Flagyl first
choice.
• If Previous hospitalization Timentin, Zosyn,
carbapenem, a fluoroquinolone, or an
aminoglyciside should be substituted for
Unasyn/Ampicillin.
• Group a strep suspect: Clinda & PCN combo
Eikenella corrodens
• “A Fastidious, slow growing, gram negative, oxidase positive,
facultative anaerobic rod. Typically found in the mucous membranes
of the oral cavity, respiratory, gi, and gu tracts. A common pathogen
in human bite wounds which can cause exceptionally painful and
rapidly necrotic lesions…associated with abscesses of the head, neck,
as well as endocarditis, osteomylitis, and fatal gram neg sepsis”
-Rosen Derm On Journal 2005
• “Has a unique association with human bite wound infections, and has
been recovered from 15-30% of of samples…more prevalent injuries
assoc with gingival crevice (59% gingival specimens)…can act
synergistically with strep viridans and is a common cause of
osteomylitis.
-Stefanopoulos Int J Oral Maxillofac Surg 2005
Talan et al. Clin Infect Dis. 1992
• Multicenter prospective study of Southern
California ER’s.
• 50 patients with infected human bites Cx’d
• Median number isolates was 4
• Eikenella isolated 30%
Eikenella
• Uniformly multiple resistance to Clinda,
Erythromycin, Flagyl, and most
aminoglycisides
• Augmentin, fluorquinolones, second or
third generation cephalosporins, or PCN to
treat. (No randomized comparative trials
for human bite wounds)