it's a presentation that includes general description , pathophysiology and management of Necrotising Fasciitis

1. Necrotising Fasciitis
Dr Anang Pangeni
068.09.

2.  Recognized and reported for centuries
 Hippocrates in the 5th century BC
 Joseph Jones in 1871 : ‘hospital gangrene’
 Meleny , 1924 , Beijing outbreak “hemolytic streptococcal
gangrene”
 Wilson , 1952, coined the term
 infection, necrosis of the fascia and subcutaneous tissue with
relative sparing of the underlying muscle

3.  A rapidly progressive tissue infection characterized
by extensive necrosis of the subcutaneous fat and
fascia with secondary involvement of skin and
rarely muscles
 Necrotizing fasciitis is a severe, insidiously
advancing, soft-tissue infection characterized by
widespread fascial necrosis

4.  High mortality
 Reported incidence 6 to 76%
 Studies* :Delay in diagnosis and consequent delayed
debridement is often the cause
 A common admission in our facility.
McHenry CR, Piotrowski JJ, Petrinic D, Malangoni MA. Determinants of mortality in necrotizing soft tissue infections. Ann Surg 1995; 221:558–563.
Wong CH, Chang HC, Pasupathy S, et al. Necrotizing fasciitis: clinical presentation, microbiology and determinants of mortality. J Bone Joint Surg
Am 2003; 85A:1454–1460.

5.  Common diagnosis in our ward
 Last 6 months data
 Commonest pathogen Staph aureus
 Others
 Enterobacter / acinetobacter / proteus /e coli
 Streptococcus interestingly not reported! Fallacies?
Total cases Male Female Mortality
51 30 21 1
Cultures sterile Monomicrobial Polymicrobial SNR
12 34 8 8

6.  Not fully understood, and in many cases no identifiable
cause can be found.
 True risk factors for NSTI have not been identified
 Agreed : pre-existing conditions that render them
susceptible to infection
 injection drug use
 chronic debilitating comorbidities (e.g.,diabetes mellitus,
immune suppression,and obesity)

7.  Cases without a recognized precipitating factor are more
likely to be caused by group A streptococcal infection,
and community-acquired MRS infection*
*Miller LG, Perdreau-Remington F, Rieg G, et al. Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcus
aureus in Los Angeles. N Engl J Med 2005; 352:1445–53.

8.  Diabetes
 Chronic disease
 Drugs—for example, steroids
 Malnutrition
 Immunosuppression
 Age > 60
 Intravenous drug misuse
 Peripheral vascular disease
 Renal failure
 Underlying malignancy
 Obesity

9.  Blunt or penetrating trauma
 Soft tissue infections
 Surgery
 Intravenous drug use
 Childbirth
 Burns
 Muscle injuries
 Minor trauma
 Insect bite,
 Pustule
 Minor operations,
 Anorectal abscess,
 Instrumentation,
 Septic abortion,
 Genitourinary infection

10.  Gram positive aerobic
bacteria
 Group A ß haemolytic
streptoccoci
 Group B streptococci
 Enterococci
 Coagulase negative
staphylococci
 Staphylococcus aureus
 Bacillus species
 Gram negative aerobic
bacteria
 Escherichia coli
 Pseudomonas aeruginosa
 Proteus species
 Serratia species
 Anaerobic bacteria
 Bacteroides species
 Clostridium species
 Peptostreptococcus species
 Fungi
 Zygomycetes
 Aspergillus
 Candida
 Other
 Vibrio species

11.  Type 1
 Polymicrobial (aerobic and anaerobic bacteria)
 Occur most commonly after surgery or in
individuals with diabetes and peripheral vascular
disease.
 Primarily includes 3 categories (locations) of
infection
 Diabetes Mellitus- infections of the feet
 Cervical necrotizing fasciitis- infection of the neck
 Fournier’s Gangrene- infection of the perineum

13.  Type 2
 A monomicrobial infection caused primarily by group
A streptococcus (GAS), although it is occasionally
caused by community-associated methicillin-resistant
Staphylococcus aureus (MRSA)
 Type 3 (not usually described)
 Clostridial gas gangrene / Vibrio spp infection

14. Bacteria proliferate within the superficial
fascia and elaborate enzymes and toxins
Expression of bacterial enzymes
such as hyaluronidase, which
degrades the fascia
Angiothrombotic microbial
invasion and liquefactive
necrosis of the superficial fascia.

15. Necrosis of the superficial fascia
Polymorphonuclear infiltration of
the deep dermis and fascia
Thrombosis and suppuration of
the veins and arteries coursing
through the fascia
Microorganism proliferation
within the destroyed fascia.

16. Occlusion of perforating nutrient vessels
to the skin causes progressive skin
ischemia.
Initially, horizontal phase predominates with rapid
spread through the fascia with extensive undermining of
the apparently normal looking skin.
Ischemic necrosis of the skin ensues with
gangrene of the subcutaneous fat, dermis
and epidermis, manifesting progressively
as bullae formation, ulceration and skin
necrosis

17. one microorganism produces the
enzymes necessary to cause
coagulation of the nutrient vessels 
tissue oxygen tension falls
tissue hypoxia allows growth of facultative
anaerobes and microaerophilic organisms
produce enzymes (eg, lecithinase,
collagenase), which lead to digestion
of fascial barriers, thus fueling the
rapid extension of the infection

18.  Early on in the evolution, the disease is clinically indistinguishable
from severe soft tissue infection such as cellulitis and erysipelas
presenting with only pain, tenderness and warm skin.
 Blistering or bullae formation is rarely seen in erysipelas or
cellulitis and should raise the suspicion of necrotizing soft tissue
infection!!
Unfortunately these ‘HARD SIGNS’ are late!

19.  Although the following features can occur with
cellulitis, they may instead suggest necrotizing
fasciitis:
 Rapid progression
 Poor therapeutic response
 Blistering necrosis
 Cyanosis
 Extreme local tenderness
 High temperature
 Tachycardia
 Hypotension
 Altered level of consciousness

20.  Early findings
 Pain
 Cellulitis
 Pyrexia
 Tachycardia
 Swelling
 Induration
 Skin anaesthesia
 Late findings
 Severe pain
 Skin discoloration (purple or
black)
 Blistering
 Haemorrhagic bullae
 Crepitus
 Discharge of “dishwater”
fluid
 Severe sepsis or SIRS
 Multiorgan failure

21. Stage I Stage II Stage III
Tenderness to
palpation(exending beyond
the apparent area of skin)
Blister or bullae formation
(serous fluid)
Hemorrhagic bullae
Erythema Skin fluctuance Skin Anesthesia
Swelling Skin induration Crepitus
Warm to palpation Skin necrosis with dusky
discoloration prgressing to
frank gangrene

22. Wong CH, Khin LW, Heng KS, Tan KC, Low CO., Journal of critical care medicine The LRINEC (Laboratory Risk Indicator for Necrotizing
Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections.epartment of Plastic Surgery, Singapore
General Hospital, Singapore.
Variables 0 1 2 3 4
WCC /mm3 <15 15-25 >25
CRP (mg/L) <150 >150
Hb (g/dl) >13.5 11-13.5 <11
Na (mmol/L) >135 <135
Creatinine(mg/
dL)
<1.6 >1.6
Glucose (g/dL) <180 >180
•PPV of 92%
• NPV of 96%.
Laboraotry Risk Indicator for Necrotising fasciitis

23.  Laboratory investigations
 Leucocytosis
 Acidosis
 Altered coagulation profile
 Hypoalbuminaemia
 Abnormal renal function
 Plain radiography
 Soft tissue gas
 CT/MRI
 May delineate extent of disease
 Soft tissue gas
 Incisional exploration or biopsy (can be done at
bedside)
 Histological confirmation of diagnosis
 Tissue culture to identify pathogens and sensitivities

24.  Gray necrotic tissue
 Lack of bleeding
 Thrombosed vessels
 “Dishwater” pus,
 Non-contracting muscle
 Positive “finger test” result
 characterized by lack of resistance to finger
dissection in normally adherent tissues

27.  Preoperative resuscitation
 Should be aggressive!
 Surgical Wound excision
 As soon as confirmed.
 Some advocate surgery as a means for diagnosis
 Clinical and laboratory findings are still not conclusive
 Diagnosis of NSTI is still a possiblity
 Aggressive Is Better!
 Researches have clearly shown the impact of early and
complete debridement on final outcome in patients with
NSTI *
 Earlier and Complete Vs Delayed or Incomplete excision
McHenry CR, Piotrowski JJ, Petrinic D, Malangoni MA. Determinants of mortality for necrotizing soft-tissue infections. Ann Surg 1995; 221:
558–63; discussion 563–5
Bilton BD, Zibari GB, McMillan RW, Aultman DF, Dunn G, McDonald JC. Aggressive surgical management of necrotizing fasciitis serves to
decrease mortality: a retrospective study. Am Surg 1998; 64:397–400;discussion 400–1.

28.  Extent of Excision
 Generous incision at outset
 Increase as demanded by the nature of tissue beneath
 Macroscopic findings are used as guide
 Occasionally, amputation of a limb is necessary to
achieve this goal and is encouraged if that is the case.
 Healthy, viable, bleeding tissue should be present at
the edges of the excision site

29.  We have not seen these!
 Advocated by different groups that argue for a
decreased number of debridements and decreased
mortality*
 increases the normal oxygen saturation in the
infected wounds by 1000-fold leading to
 Bacteriocidal effect,
 Improves neutrophil function,
 Enhanced wound healing
 Results are contradictory!
 Where available
 Should not jeopardize the standard therapy — adequate
and timely debridements
*Riseman JA, Zamboni WA, Curtis A, Graham DR, Konrad HR,Ross DS. Hyperbaric oxygen therapy for necrotizing
fasciitis reduces mortality and the need for debridements. Surgery 1990; 108:847–50.
Jallali N, Withey S, Butler PE. Hyperbaric oxygen as adjuvant therapy in the management of necrotizing fasciitis. Am J
Surg 2005; 189:462–6.

30.  Defined as infections of any of the layers within
the soft tissue compartment (dermis,subcutaneous
tissue, superficial fascia, deep fascia, or muscle)
that are associated with necrotizing changes.
 Different terms are used to define and classify
STIs, leading to confusion when referring to
infections that have common pathophysiological
and clinical characteristics and, most importantly,
share a common management strategy

31.  Necrotising fasciitis is potentially fatal condition and
can affect any part of the body .
 The aetiology is not fully understood but most patients
who develop necrotising fasciitis have pre-existing
conditions that render them susceptible to infection
 Diagnosis is often delayed because of the paucity of
symptoms and the unfamiliarity of the condition
among clinicians

32.  Laboratory findings and other diagnostic tests may be
useful adjuncts, but the diagnosis is still primarily a
clinical one and a high index of suspicion is required
 Management should consist of immediate
resuscitation, early surgical debridement, and
administration of broad spectrum intravenous
antibiotics.
 ‘Necrotising soft tissue infection’ can be used as a
standard term to designate these infections, so as to
help in correct data interpretation.