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Necrotising Fascitis

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35 views33 pages

Necrotising Fascitis

Uploaded by

drsanthoshrsk
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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NECROTISING FASCITIS

Objectives

At the end of the Lecture

 Appreciate the high mortality associated


with necrotizing fasciitis

 Explain the pathophysiology of necrotizing


fasciitis

 Describe the main challenges in the


2
diagnosis of necrotizing fasciitis
Skin and Soft Tissue Infections
 Skin and soft tissue infections (SSTIs)
are incredibly common in both
pediatric and adult medicine
 SSTIs involve suppurative bacterial or
fungal invasion of the epidermis,
dermis, or subcutaneous tissues
 SSTIs can range in severity from
benign to very serious (as in this
case)

3
History and Features
 Hippocrates first alluded to a clinical
condition of ʺnecrotizing erysipilasʺ in
the 5th century BC as a complication of
erysipelas
 Since then, numerous terms have been
applied to this condition—phagedena
gangrenosum, hospital gangrene,
Meleney gangrene, and Fournier
gangrene
 Dominant feature is inflammation and
necrosis of subcutaneous fat and deep
4
fascia, with sparing of muscle, leading
Epidemiology
 Necrotizing fasciitis is a rare disease
 The incidence of NF progressively
increases among patients aged 50 years
and older
 Necrotizing fasciitis generally affects
patients with chronic illnesses
 More than half of patients have pre-existing
medical conditions and 35% have at least two
 Despite improved recognition, NF
continues to be associated with a high
mortality—in the past decade, reported to
5
be between 15% to 45%
INCIDENCE

 Rare disease
 Incidence: 1000 cases/year, 0.04
cases/1000 person-years (U.S.A)
 Increased incidence 1980 -2000
 Prevalence: one or two cases/career
for average practitioner.
Classification

Classification Factor Comment

Anatomic location Fournier’s gangrene


perineum/scrotum

Depth of Infection Necrotizing adipositis (most


(correlates with mortality) common), fasciitis, myositis.

Microbial cause Type I: polymicrobial (most


common, 55-75%)
Type II: Monomicrobial: (staph,
strep, clostridia).
Type III: Vibrio vulnificus
Microbiology/ Risk Factors
Type I

 Most common ( 55-75%).


 Polymicrobial (GPC, GNR, Anaerobes).
 C. Perfingens rare cause of NSTI.
 Perineum- trunk.
 Immunocompromised patients (DM, PVD).
 IV drug use.
 No inciting event for 20 to 50 % of
patients.
Microbiology/ Risk Factors
Type I
 Immunocompromised patients
 Obesity
 Chronic Renal Failure
 HIV
 Alcohol abuse
 Abscess
 IV drugs
 Trauma (blunt/penetrating)
 Insect bites
 Surgical incisions
 Indwelling catheters
 Chicken pox
 Perforation of GI tract (clostridium septicum)
Microbiology/ Risk Factors
Type II
 Group A Streptococcus (pyogenes): can
survive in macrophage.
 Staphylococcus Aureus
 Association with Toxic Shock Syndrome.
 MRSA soft tissue infection cultured in up to
40% necrotic wounds ( IV drug abusers)
 Healthy, young, immunocompetent hosts.
 Location: extremities .
 Trauma or operation.
Microbiology/ Risk Factors
Type III
 Least common type
 Vibrio vulnificus
 Skin break
 Warm sea water
 Coastal communities
 Risk factor: chronic HBV
 Fulminant course
Pathophysiology of NF
 Microbial
invasion of the
subcutaneous tissues occurs either
through:
1) External trauma
2) Direct spread from a perforated viscus
3) From a hematogenous source
 NFcan affect any part of the body;
extremities and the perineum are
most commonly affected

12
Pathophysiology of NF
 As infection progresses, the skin becomes
more tense and red with indistinct margins
 Local pain is replaced by numbness (from
compression or infarction of nerves)
 Next, skin becomes pale, then mottled and
purple looking, and finally gangrenous
 If gas-forming bacteria are present, air under
the skin (crepitus) may be palpated

13
Evolution of Physical Signs in NF
 A clinical staging of the disease has been
proposed based on cutaneous signs (see
below)
 Symptoms may occur over hours to days
and patients may present with sepsis or
Stage 1 (early) Stage 2 Stage 3 (late)
septic shock (intermediate)
Warm to palpation Blister or bullae Hemorrhagic bullae
formation (serous
fluid)
Erythema Skin fluctuance Skin anesthesia
Tenderness to palpitation Skin induration Crepitus
(extending beyond
apparent areas of skin
involvement)
Swelling Skin necrosis with dusky
14 discoloration progressing to
frank gangrene
Differential Diagnosis
Disorder Characteristic

Cellulitis/adipositis Erythematous edematous tissue


with normal subc. fat and fascia

Myonecrosis Noninfectious inflammation/


necrosis of muscle only

Noninfectious fasciitis Chronic disorder, Dx. biopsy,


Tx. Steroids

Phlegmasia cerulea Edema of entire affected extremity


dolens
Myxedema Systemic manifestations of severe
hypothyroidism
Early Diagnosis of NF
 Early diagnosis and adequate
debridement within 24 hours are the
most important factors impacting
survival
 Patients who receive surgery in the first
24 hours have mortality rate of 4.2%
−6.7%
 Delaying surgery more than 24 hours is
associated with mortality rates of 23%
−75%
16
Challenges in Diagnosis
 Earlydiagnosis of
necrotizing fasciitis (NF) is
notoriously difficult and
misdiagnosis is common
 In one study, NF was initially
misdiagnosed 71.4% of the
time

17
Challenges in Diagnosis

 Multiple factors contribute to missed or


delayed diagnosis:
 NF is a rare disease and many practitioners
may be encountering it for the first time
 NF initially can present similarly to other
common soft tissue infections (as in this
patient where it appeared he had simple
bruising after his fall)
 The cutaneous signs of NF usually lag behind
disease pathology
 Systemic signs of NF may not correlate with
18the cutaneous signs and vice versa; patients
Challenges in Diagnosis
 Theʺhard signsʺ (e.g., bullae,
numbness, crepitus, and skin
necrosis) may be absent
 In one study, they were present in only
43% of patients with NF
 Fever may not be present
 In one review, only 32%−56% of patients
with NF had a fever
 In
addition, initial symptoms of NF
can be mild until the patient rapidly
deteriorates and develops septic
19
Strategies to Improve Diagnosis
 Multiple specific strategies may help
prevent missing a diagnosis of NF
 Recognize pain out of proportion
to the skin manifestations is a
consistent feature of NF
 Inthis case, the patient's severe
pain requiring increasing
intravenous opiates and a PCA
pump should have been a sign that
this was a more serious infection
20
Strategies to Improve Diagnosis
 RecognizeNF often has rapid
progression of infection with
migration of the margins of
erythema and skin induration
despite use of antibiotics

 Thisextension can progress over


the course of hours
Strategies to Improve Diagnosis

 Threeother cutaneous features can


serve as diagnostic clues:
1) Margins may be indistinct and poorly
defined
2) Tenderness may extend beyond the
apparent involved area of skin
3) Lymphangitis (inflammation of lymphatics,
seen as streaking along skin) is rarely
seen in NF

22
Strategies to Improve Diagnosis

 Use of clinical pathways may also


help aid in diagnoses
 Institutions should involve
multidisciplinary teams (often
including surgeons, infectious disease
specialists, and wound care experts)
 Education of frontline clinicians is
also crucial
Treatment
Surgical Debridement (SD)
 Cornerstone of therapy.
 Delayed SD for more than 24 h is associated with
a nine fold increase in mortality (Wong and
colleagues)
 Wide excision to comprise healthy, bleeding
tissue.
 Serial debridements ( 3 spaced 12 to 36 hrs.)
 Amputation is a consideration ( IV drug users).
 Diverting colostomy for perineal/perianal NSTI
 Open wound , wet to dry dressings.
 Wound vac.
 Skin grafting for large wounds.
Operative Findings
 Operative exploration is the gold
standard modality for diagnosis of NSTI
 “Dishwater” or foul-smelling discharge
 Necrosis
 Lack of bleeding
 Loss of normal resistance to the fascia.
 Biopsy from interface between live and
dead tissue is rarely indicated.
Treatment
 IV ABXs: Vancomycin, Linezolid, Daptomycin,
quinupristin/dalfopristin, clindamycin ( G+)
Clindamycin (anaerobes)
Quinolones ( G-)
 IV IG: binds staph/strep toxins limiting
SIRS.
Not FDA approved.
Critically ill patients from staph. or strept.

 Hyperbaric O2: controversial and unproved.


inhibits toxin elaboration by
clostridia, increases local
O2 tension and killing ability
of leukocytes.
Morbidity and Mortality

 Timing of operation the most critical


determinant.
 Consider age, comorbidities, DM,
shock, ARF, coagulopathy….
 Morbidity as high as 82% (Eliot et all)
 Amputation rate 15 to 30%
 Complications: nosocomial infections,
respiratory failure, ARDS, ARF,
seizures, stroke, cardiac arrest….
Take-Home Points
 Early diagnosis of necrotizing fasciitis and early
debridement is crucial to survival and reduction in
morbidity and need for amputation
 Early presenting signs of necrotizing fasciitis can be
non-specific
 Pain out of proportion to what one would expect for
simple cellulitis should ring alarm bells and prompt
physicians to expand the differential diagnosis to
include NF
 There is an evolution of clinical signs of necrotizing
fasciitis—from early to late stages
 A keen sense of suspicion and constant review of a
patient are the only ways to reliably detect necrotizing
fasciitis at an early stage
28

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